The original member of the family of endothelial cell growth factors referred to as VASCULAR ENDOTHELIAL GROWTH FACTORS. Vascular endothelial growth factor-A was originally isolated from tumor cells and referred to as "tumor angiogenesis factor" and "vascular permeability factor". Although expressed at high levels in certain tumor-derived cells it is produced by a wide variety of cell types. In addition to stimulating vascular growth and vascular permeability it may play a role in stimulating VASODILATION via NITRIC OXIDE-dependent pathways. Alternative splicing of the mRNA for vascular endothelial growth factor A results in several isoforms of the protein being produced.
A family of angiogenic proteins that are closely-related to VASCULAR ENDOTHELIAL GROWTH FACTOR A. They play an important role in the growth and differentiation of vascular as well as lymphatic endothelial cells.
These growth factors are soluble mitogens secreted by a variety of organs. The factors are a mixture of two single chain polypeptides which have affinity to heparin. Their molecular weight are organ and species dependent. They have mitogenic and chemotactic effects and can stimulate endothelial cells to grow and synthesize DNA. The factors are related to both the basic and acidic FIBROBLAST GROWTH FACTORS but have different amino acid sequences.
A 200-230-kDa tyrosine kinase receptor for vascular endothelial growth factors found primarily in endothelial and hematopoietic cells and their precursors. VEGFR-2 is important for vascular and hematopoietic development, and mediates almost all endothelial cell responses to VEGF.
A family of closely related RECEPTOR PROTEIN-TYROSINE KINASES that bind vascular endothelial growth factors. They share a cluster of seven extracellular Ig-like domains which are important for ligand binding. They are highly expressed in vascular endothelial cells and are critical for the physiological and pathological growth, development and maintenance of blood and lymphatic vessels.
Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity.
A 180-kDa VEGF receptor found primarily in endothelial cells that is essential for vasculogenesis and vascular maintenance. It is also known as Flt-1 (fms-like tyrosine kinase receptor-1). A soluble, alternatively spliced isoform of the receptor may serve as a binding protein that regulates the availability of various ligands for VEGF receptor binding and signal transduction.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
Cell surface receptors that bind growth or trophic factors with high affinity, triggering intracellular responses which influence the growth, differentiation, or survival of cells.
A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR D in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.
A vascular endothelial cell growth factor receptor whose expression is restricted primarily to adult lymphatic endothelium. VEGFR-3 preferentially binds the vascular endothelial growth factor C and vascular endothelial growth factor D and may be involved in the control of lymphangiogenesis.
Agents and endogenous substances that antagonize or inhibit the development of new blood vessels.
A vascular endothelial growth factor that specifically binds to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2 and VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-3. In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR C in that they both contain N- and C-terminal extensions that were not found in other VEGF family members.
A vascular endothelial growth factor expressed in a variety of tissues. It binds with high specificity to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-1 and NEUROPILIN-1.
A class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.
A single-chain polypeptide growth factor that plays a significant role in the process of WOUND HEALING and is a potent inducer of PHYSIOLOGIC ANGIOGENESIS. Several different forms of the human protein exist ranging from 18-24 kDa in size due to the use of alternative start sites within the fgf-2 gene. It has a 55 percent amino acid residue identity to FIBROBLAST GROWTH FACTOR 1 and has potent heparin-binding activity. The growth factor is an extremely potent inducer of DNA synthesis in a variety of cell types from mesoderm and neuroectoderm lineages. It was originally named basic fibroblast growth factor based upon its chemical properties and to distinguish it from acidic fibroblast growth factor (FIBROBLAST GROWTH FACTOR 1).
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Dimeric cell surface receptor involved in angiogenesis (NEOVASCULARIZATION, PHYSIOLOGICAL) and axonal guidance. Neuropilin-1 is a 140-kDa transmembrane protein that binds CLASS 3 SEMAPHORINS, and several other growth factors. Neuropilin-1 forms complexes with plexins or VEGF RECEPTORS, and binding affinity and specificity are determined by the composition of the neuropilin dimer and the identity of other receptors complexed with it. Neuropilin-1 is expressed in distinct patterns during neural development, complementary to those described for NEUROPILIN-2.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
Agents that induce or stimulate PHYSIOLOGIC ANGIOGENESIS or PATHOLOGIC ANGIOGENESIS.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The first to be discovered member of the angiopoietin family. It may play a role in increasing the sprouting and branching of BLOOD VESSELS. Angiopoietin-1 specifically binds to and stimulates the TIE-2 RECEPTOR. Several isoforms of angiopoietin-1 occur due to ALTERNATIVE SPLICING of its mRNA.
A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
An angiopoietin that is closely related to ANGIOPOIETIN-1. It binds to the TIE-2 RECEPTOR without receptor stimulation and antagonizes the effect of ANGIOPOIETIN-1. However its antagonistic effect may be limited to cell receptors that occur within the vasculature. Angiopoietin-2 may therefore play a role in down-regulation of BLOOD VESSEL branching and sprouting.
A condition of decreased oxygen content at the cellular level.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
Proteins produced by organs of the mother or the PLACENTA during PREGNANCY. These proteins may be pregnancy-specific (present only during pregnancy) or pregnancy-associated (present during pregnancy or under other conditions such as hormone therapy or certain malignancies.)
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
The minute vessels that connect the arterioles and venules.
A cell line derived from cultured tumor cells.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A basic helix-loop-helix transcription factor that plays a role in APOPTOSIS. It is composed of two subunits: ARYL HYDROCARBON RECEPTOR NUCLEAR TRANSLOCATOR and HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.
Cell adhesion molecules present on virtually all monocytes, platelets, and granulocytes. CD31 is highly expressed on endothelial cells and concentrated at the junctions between them.
The formation of LYMPHATIC VESSELS.
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is PROTO-ONCOGENE PROTEINS C-MET.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Mitogenic peptide growth hormone carried in the alpha-granules of platelets. It is released when platelets adhere to traumatized tissues. Connective tissue cells near the traumatized region respond by initiating the process of replication.
Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina.
A TIE receptor tyrosine kinase that is found almost exclusively on ENDOTHELIAL CELLS. It is required for both normal embryonic vascular development (NEOVASCULARIZATION, PHYSIOLOGIC) and tumor angiogenesis (NEOVASCULARIZATION, PATHOLOGIC).
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Intercellular signaling peptides and proteins that regulate the proliferation of new blood vessels under normal physiological conditions (ANGIOGENESIS, PHYSIOLOGICAL). Aberrant expression of angiogenic proteins during disease states such as tumorigenesis can also result in PATHOLOGICAL ANGIOGENESIS.
Endothelial cells that line venous vessels of the UMBILICAL CORD.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
New blood vessels originating from the corneal veins and extending from the limbus into the adjacent CORNEAL STROMA. Neovascularization in the superficial and/or deep corneal stroma is a sequel to numerous inflammatory diseases of the ocular anterior segment, such as TRACHOMA, viral interstitial KERATITIS, microbial KERATOCONJUNCTIVITIS, and the immune response elicited by CORNEAL TRANSPLANTATION.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Signal molecules that are involved in the control of cell growth and differentiation.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Elements of limited time intervals, contributing to particular results or situations.
A well-characterized basic peptide believed to be secreted by the liver and to circulate in the blood. It has growth-regulating, insulin-like, and mitogenic activities. This growth factor has a major, but not absolute, dependence on GROWTH HORMONE. It is believed to be mainly active in adults in contrast to INSULIN-LIKE GROWTH FACTOR II, which is a major fetal growth factor.
A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.
Established cell cultures that have the potential to propagate indefinitely.
Tubular vessels that are involved in the transport of LYMPH and LYMPHOCYTES.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Relatively complete absence of oxygen in one or more tissues.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
The relationship between the dose of an administered drug and the response of the organism to the drug.
In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The blood vessels which supply and drain the RETINA.
An EPIDERMAL GROWTH FACTOR related protein that is found in a variety of tissues including EPITHELIUM, and maternal DECIDUA. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form which binds to the EGF RECEPTOR.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
Transmembrane receptor for CLASS 3 SEMAPHORINS and several vascular endothelial growth factor isoforms. Neuropilin-2 functions either as a homodimer or as a heterodimer with NEUROPILIN-1. The binding affinity of neuropilin-2 varies for different class 3 semaphorin isoforms and is dependent on the composition of the dimer. The protein also forms receptor complexes with plexins and with VEGF RECEPTORS, which alters the binding characteristics of the receptor.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.
Culture media containing biologically active components obtained from previously cultured cells or tissues that have released into the media substances affecting certain cell functions (e.g., growth, lysis).
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME.
Restoration of integrity to traumatized tissue.
Proteins prepared by recombinant DNA technology.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Transplantation between animals of different species.
A highly vascularized extra-embryonic membrane, formed by the fusion of the CHORION and the ALLANTOIS. It is mostly found in BIRDS and REPTILES. It serves as a model for studying tumor or cell biology, such as angiogenesis and TISSUE TRANSPLANTATION.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
Angiostatic proteins that are formed from proteolytic cleavage of COLLAGEN TYPE XVIII.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Antibodies produced by a single clone of cells.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Hormonally active polypeptides that can induce the transformed phenotype when added to normal, non-transformed cells. They have been found in culture fluids from retrovirally transformed cells and in tumor-derived cells as well as in non-neoplastic sources. Their transforming activities are due to the simultaneous action of two otherwise unrelated factors, TRANSFORMING GROWTH FACTOR ALPHA and TRANSFORMING GROWTH FACTOR BETA.
Agents that inhibit PROTEIN KINASES.
Glycoprotein molecules on the surface of B- and T-lymphocytes, that react with molecules of antilymphocyte sera, lectins, and other agents which induce blast transformation of lymphocytes.
Unique slender cells with multiple processes extending along the capillary vessel axis and encircling the vascular wall, also called mural cells. Pericytes are imbedded in the BASEMENT MEMBRANE shared with the ENDOTHELIAL CELLS of the vessel. Pericytes are important in maintaining vessel integrity, angiogenesis, and vascular remodeling.
The finer blood vessels of the vasculature that are generally less than 100 microns in internal diameter.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Tumors or cancer of the LUNG.
A vascular endothelial growth factor whose expression is found largely restricted to the GONADS; ADRENAL CORTEX; and PLACENTA. It has similar biological activity to VASCULAR ENDOTHELIAL GROWTH FACTOR-A.
Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.
A pathological process consisting of the formation of new blood vessels in the CHOROID.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.
Compounds that include the amino-N-phenylamide structure.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
An extracellular matrix glycoprotein from platelets and a variety of normal and transformed cells of both mesenchymal and epithelial origin. Thrombospondin-1 is believed to play a role in cell migration and proliferation, during embryogenesis and wound repair. Also, it has been studied for its use as a potential regulator of tumor growth and metastasis.
Organic salts and esters of benzenesulfonic acid.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
Tumors or cancers of the KIDNEY.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Mode of communication wherein a bound hormone affects the function of the cell type that produced the hormone.
Specific molecular sites or structures on cell membranes that react with FIBROBLAST GROWTH FACTORS (both the basic and acidic forms), their analogs, or their antagonists to elicit or to inhibit the specific response of the cell to these factors. These receptors frequently possess tyrosine kinase activity.
Techniques and strategies which include the use of coding sequences and other conventional or radical means to transform or modify cells for the purpose of treating or reversing disease conditions.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Specific receptors on cell membranes that react with PLATELET-DERIVED GROWTH FACTOR, its analogs, or antagonists. The alpha PDGF receptor (RECEPTOR, PLATELET-DERIVED GROWTH FACTOR ALPHA) and the beta PDGF receptor (RECEPTOR, PLATELET-DERIVED GROWTH FACTOR BETA) are the two principle types of PDGF receptors. Activation of the protein-tyrosine kinase activity of the receptors occurs by ligand-induced dimerization or heterodimerization of PDGF receptor types.
An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.
Neuropilins are 140-kDa vertebrate cell surface receptors that bind neuronal guidance molecules during neural development and axonal outgrowth, and modulate VEGF-mediated angiogenesis. NEUROPILIN-1 and NEUROPILIN-2 differ in their binding specificities, and are distributed complementarily in regions of the developing nervous system. Neuropilins are receptors for secreted CLASS 3 SEMAPHORINS as well as for vascular endothelial growth factors, and may form hetero- or homodimers. They may also interact synergistically with plexins and with VEGF RECEPTORS to form receptor complexes with distinct affinities and specificities. Neuropilin binding specificity is determined by CUB and coagulation-factor-like domains in the extracellular portion of the molecule, while a MAM domain is essential for SIGNAL TRANSDUCTION.
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.
Tumors or cancer of the human BREAST.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and PELLAGRA. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A PDGF receptor that binds specifically to the PDGF-B chain. It contains a protein-tyrosine kinase activity that is involved in SIGNAL TRANSDUCTION.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A fibroblast growth factor receptor with specificity for FIBROBLAST GROWTH FACTORS; HEPARAN SULFATE PROTEOGLYCAN; and NEURONAL CELL ADHESION MOLECULES. Several variants of the receptor exist due to multiple ALTERNATIVE SPLICING of its mRNA. Fibroblast growth factor receptor 1 is a tyrosine kinase that transmits signals through the MAP KINASE SIGNALING SYSTEM.
Cellular signaling in which a factor secreted by a cell affects other cells in the local environment. This term is often used to denote the action of INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS on surrounding cells.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A malignant epithelial tumor with a glandular organization.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A 17-kDa single-chain polypeptide growth factor that plays a significant role in the process of WOUND HEALING and is a potent inducer of PHYSIOLOGIC ANGIOGENESIS. It binds to HEPARIN, which potentiates its biological activity and protects it from proteolysis. The growth factor is an extremely potent inducer of DNA synthesis in a variety of cell types from mesoderm and neuroectoderm lineages, and also has chemotactic and mitogenic activities. It was originally named acidic fibroblast growth factor based upon its chemical properties and to distinguish it from basic fibroblast growth factor (FIBROBLAST GROWTH FACTOR 2).
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
A CCN protein family member that regulates a variety of extracellular functions including CELL ADHESION; CELL MIGRATION; and EXTRACELLULAR MATRIX synthesis. It is found in hypertrophic CHONDROCYTES where it may play a role in CHONDROGENESIS and endochondral ossification.
A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.
The transparent, semigelatinous substance that fills the cavity behind the CRYSTALLINE LENS of the EYE and in front of the RETINA. It is contained in a thin hyaloid membrane and forms about four fifths of the optic globe.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
A system of organs and tissues that process and transport immune cells and LYMPH.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
The transparent anterior portion of the fibrous coat of the eye consisting of five layers: stratified squamous CORNEAL EPITHELIUM; BOWMAN MEMBRANE; CORNEAL STROMA; DESCEMET MEMBRANE; and mesenchymal CORNEAL ENDOTHELIUM. It serves as the first refracting medium of the eye. It is structurally continuous with the SCLERA, avascular, receiving its nourishment by permeation through spaces between the lamellae, and is innervated by the ophthalmic division of the TRIGEMINAL NERVE via the ciliary nerves and those of the surrounding conjunctiva which together form plexuses. (Cline et al., Dictionary of Visual Science, 4th ed)
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.
A nonmuscle isoform of myosin type II found predominantly in neuronal tissue.
The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.
An extra-embryonic membranous sac derived from the YOLK SAC of REPTILES; BIRDS; and MAMMALS. It lies between two other extra-embryonic membranes, the AMNION and the CHORION. The allantois serves to store urinary wastes and mediate exchange of gas and nutrients for the developing embryo.
A family of structurally-related angiogenic proteins of approximately 70 kDa in size. They have high specificity for members of the TIE RECEPTOR FAMILY.
A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.
A well-characterized neutral peptide believed to be secreted by the LIVER and to circulate in the BLOOD. It has growth-regulating, insulin-like and mitogenic activities. The growth factor has a major, but not absolute, dependence on SOMATOTROPIN. It is believed to be a major fetal growth factor in contrast to INSULIN-LIKE GROWTH FACTOR I, which is a major growth factor in adults.
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.
A ubiquitin-protein ligase that mediates OXYGEN-dependent polyubiquitination of HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT. It is inactivated in VON HIPPEL-LINDAU SYNDROME.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
A 44-kDa extracellular signal-regulated MAP kinase that may play a role the initiation and regulation of MEIOSIS; MITOSIS; and postmitotic functions in differentiated cells. It phosphorylates a number of TRANSCRIPTION FACTORS; and MICROTUBULE-ASSOCIATED PROTEINS.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
The administration of substances into the VITREOUS BODY of the eye with a hypodermic syringe.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.
A fibroblast growth factor that is a specific mitogen for EPITHELIAL CELLS. It binds a complex of HEPARAN SULFATE and FIBROBLAST GROWTH FACTOR RECEPTOR 2B.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.
The main trunk of the systemic arteries.
Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.
A mitogen-activated protein kinase subfamily that is widely expressed and plays a role in regulation of MEIOSIS; MITOSIS; and post mitotic functions in differentiated cells. The extracellular signal regulated MAP kinases are regulated by a broad variety of CELL SURFACE RECEPTORS and can be activated by certain CARCINOGENS.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The outermost extra-embryonic membrane surrounding the developing embryo. In REPTILES and BIRDS, it adheres to the shell and allows exchange of gases between the egg and its environment. In MAMMALS, the chorion evolves into the fetal contribution of the PLACENTA.
Cellular DNA-binding proteins encoded by the sis gene (GENES, SIS). c-sis proteins make up the B chain of PLATELET-DERIVED GROWTH FACTOR. Overexpression of c-sis causes tumorigenesis.

VEGF is required for growth and survival in neonatal mice. (1/12040)

We employed two independent approaches to inactivate the angiogenic protein VEGF in newborn mice: inducible, Cre-loxP- mediated gene targeting, or administration of mFlt(1-3)-IgG, a soluble VEGF receptor chimeric protein. Partial inhibition of VEGF achieved by inducible gene targeting resulted in increased mortality, stunted body growth and impaired organ development, most notably of the liver. Administration of mFlt(1-3)-IgG, which achieves a higher degree of VEGF inhibition, resulted in nearly complete growth arrest and lethality. Ultrastructural analysis documented alterations in endothelial and other cell types. Histological and biochemical changes consistent with liver and renal failure were observed. Endothelial cells isolated from the liver of mFlt(1-3)-IgG-treated neonates demonstrated an increased apoptotic index, indicating that VEGF is required not only for proliferation but also for survival of endothelial cells. However, such treatment resulted in less significant alterations as the animal matured, and the dependence on VEGF was eventually lost some time after the fourth postnatal week. Administration of mFlt(1-3)-IgG to juvenile mice failed to induce apoptosis in liver endothelial cells. Thus, VEGF is essential for growth and survival in early postnatal life. However, in the fully developed animal, VEGF is likely to be involved primarily in active angiogenesis processes such as corpus luteum development.  (+info)

Role of alphavbeta3 integrin in the activation of vascular endothelial growth factor receptor-2. (2/12040)

Interaction between integrin alphavbeta3 and extracellular matrix is crucial for endothelial cells sprouting from capillaries and for angiogenesis. Furthermore, integrin-mediated outside-in signals co-operate with growth factor receptors to promote cell proliferation and motility. To determine a potential regulation of angiogenic inducer receptors by the integrin system, we investigated the interaction between alphavbeta3 integrin and tyrosine kinase vascular endothelial growth factor receptor-2 (VEGFR-2) in human endothelial cells. We report that tyrosine-phosphorylated VEGFR-2 co-immunoprecipitated with beta3 integrin subunit, but not with beta1 or beta5, from cells stimulated with VEGF-A165. VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin, compared with cells plated on the alpha5beta1 ligand, fibronectin or the alpha2beta1 ligand, collagen. BV4 anti-beta3 integrin mAb, which does not interfere with endothelial cell adhesion to vitronectin, reduced (i) the tyrosine phosphorylation of VEGFR-2; (ii) the activation of downstream transductor phosphoinositide 3-OH kinase; and (iii) biological effects triggered by VEGF-A165. These results indicate a new role for alphavbeta3 integrin in the activation of an in vitro angiogenic program in endothelial cells. Besides being the most important survival system for nascent vessels by regulating cell adhesion to matrix, alphavbeta3 integrin participates in the full activation of VEGFR-2 triggered by VEGF-A, which is an important angiogenic inducer in tumors, inflammation and tissue regeneration.  (+info)

Vascular endothelial growth factor activates nuclear factor of activated T cells in human endothelial cells: a role for tissue factor gene expression. (3/12040)

Vascular endothelial growth factor (VEGF) is a potent angiogenic inducer that stimulates the expression of tissue factor (TF), the major cellular initiator of blood coagulation. Here we show that signaling triggered by VEGF induced DNA-binding and transcriptional activities of nuclear factor of activated T cells (NFAT) and AP-1 in human umbilical vein endothelial cells (HUVECs). VEGF also induced TF mRNA expression and gene promoter activation by a cyclosporin A (CsA)-sensitive mechanism. As in lymphoid cells, NFAT was dephosphorylated and translocated to the nucleus upon activation of HUVECs, and these processes were blocked by CsA. NFAT was involved in the VEGF-mediated TF promoter activation as evidenced by cotransfection experiments with a dominant negative version of NFAT and site-directed mutagenesis of a newly identified NFAT site within the TF promoter that overlaps with a previously identified kappaB-like site. Strikingly, this site bound exclusively NFAT not only from nuclear extracts of HUVECs activated by VEGF, a stimulus that failed to induce NF-kappaB-binding activity, but also from extracts of cells activated with phorbol esters and calcium ionophore, a combination of stimuli that triggered the simultaneous activation of NFAT and NF-kappaB. These results implicate NFAT in the regulation of endothelial genes by physiological means and shed light on the mechanisms that switch on the gene expression program induced by VEGF and those regulating TF gene expression.  (+info)

Expression of vascular endothelial growth factor in human oral squamous cell carcinoma: its association with tumour progression and p53 gene status. (4/12040)

AIMS: To correlate vascular endothelial growth factor (VEGF) expression in oral squamous cell carcinoma with the clinicopathological characteristics and prognosis; and to assess whether p53 gene status is associated with VEGF expression in human cancers. METHODS: Tumour specimens from 45 patients with oral squamous cell carcinomas were examined. Expression of VEGF was determined using an immunohistochemical method, and a tumour was considered positive when more than 5% of the neoplastic cells showed VEGF immunoreactivity. The p53 gene status was screened using a polymerase chain reaction--single strand conformation polymorphism analysis. RESULTS: VEGF positive staining was detected in 19 (42.2%) of the 45 cases. VEGF immunoreactivity did not correlate with the histological degree of tumour differentiation, clinical stages, or lymph node metastasis. The patients with VEGF positive tumours had a significantly worse prognosis than those with VEGF negative tumours. The five year overall survival rate of the VEGF negative patients was 76.5%, as compared with 48.8% for the VEGF positive patients. No significant association between VEGF expression and the p53 gene status of the tumours was found. CONCLUSIONS: VEGF is a good prognostic indicator of the survival of patients with oral squamous cell carcinoma. The p53 gene status does not seem to be associated with VEGF expression in these cancers.  (+info)

Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (5/12040)

Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1-3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1beta mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor-BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells.  (+info)

Vascular endothelial growth factor (VEGF) receptor II-derived peptides inhibit VEGF. (6/12040)

Vascular endothelial growth factor (VEGF) directly stimulates endothelial cell proliferation and migration via tyrosine kinase receptors of the split kinase domain family. It mediates vascular growth and angiogenesis in the embryo but also in the adult in a variety of physiological and pathological conditions. The potential binding site of VEGF with its receptor was identified using cellulose-bound overlapping peptides of the extracytosolic part of the human vascular endothelial growth factor receptor II (VEGFR II). Thus, a peptide originating from the third globular domain of the VEGFR II comprising residues 247RTELNVGIDFNWEYP261 was revealed as contiguous sequence stretch, which bound 125I-VEGF165. A systematic replacement with L-amino acids within the peptide representing the putative VEGF-binding site on VEGFR II indicates Asp255 as the hydrophilic key residue for binding. The dimerized peptide (RTELNVGIDFNWEYPAS)2K inhibits VEGF165 binding with an IC50 of 0.5 microM on extracellular VEGFR II fragments and 30 microM on human umbilical vein cells. VEGF165-stimulated autophosphorylation of VEGFR II as well as proliferation and migration of microvascular endothelial cells was inhibited by the monomeric peptide RTELNVGIDFNWEYPASK at a half-maximal concentration of 3-10, 0.1, and 0.1 microM, respectively. We conclude that transduction of the VEGF165 signal can be interrupted with a peptide derived from the third Ig-like domain of VEGFR II by blockade of VEGF165 binding to its receptor.  (+info)

Expression of thrombospondin-1 in ischemia-induced retinal neovascularization. (7/12040)

Thrombospondin-1 is an extracellular matrix protein that inhibits endothelial cell proliferation, migration, and angiogenesis. This study was performed to investigate the role of thrombospondin-1 in ischemic retinal neovascularization. In a murine model of retinal neovascularization, thrombospondin-1 mRNA was increased from postnatal day 13 (P13), with a threefold peak response observed on P15, corresponding to the time of development of retinal neovascularization. Prominent expression of thrombospondin-1 was observed in neovascular cells, specifically, cells adjacent to the area of nonperfusion. It has been suggested that vascular endothelial growth factor (VEGF) plays a major role in ischemia-induced retinal neovascularization of this model, so we studied the effects of VEGF on thrombospondin-1 expression. In bovine retinal microcapillary endothelial cells, VEGF induced a biphasic response of thrombospondin-1 expression; VEGF decreased thrombospondin-1 mRNA 0.41-fold after 4 hours, whereas it increased, with a threefold peak response, after 24 hours. VEGF-induced endothelial cell proliferation was completely inhibited by exogenous thrombospondin-1 and increased by 37.5% with anti-thrombospondin-1 antibody. The present findings suggest that, in the ischemic retina, retinal neovascular cells increase thrombospondin-1 expression, and VEGF may stimulate endogenous thrombospondin-1 induction, which inhibits endothelial cell growth. VEGF-mediated thrombospondin-1 induction in ischemia-induced angiogenesis may be a negative feedback mechanism.  (+info)

Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF. (8/12040)

Diabetes is a major risk factor for coronary and peripheral artery diseases. Although diabetic patients often present with advanced forms of these diseases, it is not known whether the compensatory mechanisms to vascular ischemia are affected in this condition. Accordingly, we sought to determine whether diabetes could: 1) impair the development of new collateral vessel formation in response to tissue ischemia and 2) inhibit cytokine-induced therapeutic neovascularization. Hindlimb ischemia was created by femoral artery ligation in nonobese diabetic mice (NOD mice, n = 20) and in control C57 mice (n = 20). Hindlimb perfusion was evaluated by serial laser Doppler studies after the surgery. In NOD mice, measurement of the Doppler flow ratio between the ischemic and the normal limb indicated that restoration of perfusion in the ischemic hindlimb was significantly impaired. At day 14 after surgery, Doppler flow ratio in the NOD mice was 0.49+/-0.04 versus 0.73+/-0.06 for the C57 mice (P< or =0.005). This impairment in blood flow recovery persisted throughout the duration of the study with Doppler flow ratio values at day 35 of 0.50+/-0.05 versus 0.90+/-0.07 in the NOD and C57 mice, respectively (P< or =0.001). CD31 immunostaining confirmed the laser Doppler data by showing a significant reduction in capillary density in the NOD mice at 35 days after surgery (302+/-4 capillaries/mm2 versus 782+/-78 in C57 mice (P< or =0.005). The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry. The central role of VEGF was confirmed by showing that normal levels of neovascularization (compared with C57) could be achieved in NOD mice that had been supplemented for this growth factor via intramuscular injection of an adenoviral vector encoding for VEGF. We conclude that 1) diabetes impairs endogenous neovascularization of ischemic tissues; 2) the impairment in new blood vessel formation results from reduced expression of VEGF; and 3) cytokine supplementation achieved by intramuscular adeno-VEGF gene transfer restores neovascularization in a mouse model of diabetes.  (+info)

TY - JOUR. T1 - Coffee induces vascular endothelial growth factor (VEGF) expression in human neuroblastama SH-SY5Y cells. AU - Kakio, Shota. AU - Tago, Megumi. AU - Kobata, Kenji. AU - Tamura, Hiroomi. PY - 2016/1/21. Y1 - 2016/1/21. N2 - Recent evidence indicates that hypoxia-inducible vascular endothelial growth factor (VEGF) has neurotrophic and neuroprotective effects on neuronal and glial cells. On the other hand, recent epidemiological studies showed that daily coffee consumption has been associated with a lower risk of several neuronal disorders. Therefore, we investigated the effect of coffee on VEGF expression in human neuroblastoma SH-SY5Y cells. We found that even low concentration of coffee (. AB - Recent evidence indicates that hypoxia-inducible vascular endothelial growth factor (VEGF) has neurotrophic and neuroprotective effects on neuronal and glial cells. On the other hand, recent epidemiological studies showed that daily coffee consumption has been associated with a lower risk ...
Table of Contents. Table of Contents 2. List of Tables 5. List of Figures 5. Introduction 6. Global Markets Direct Report Coverage 6. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF) Overview 7. Therapeutics Development 8. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF)-Products under Development by Stage of Development 8. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF)-Products under Development by Therapy Area 9. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF)-Products under Development by Indication 10. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF)-Pipeline Products Glance 11. Late Stage Products 11. Early Stage Products 12. Placenta Growth Factor (Vascular Endothelial Growth Factor Related Protein or PGF)-Products under Development by Companies 13. Placenta Growth Factor (Vascular Endothelial Growth Factor Related ...
Background: The development of biomarkers predictive of response to immune checkpoint inhibitor (ICI) therapies in advanced melanoma is an area of great interest in oncology. Our study evaluated the potential role of serum vascular endothelial growth factor (VEGF) as a predictive biomarker of clinical benefit and response to treatment with ICIs.Methods: Pre-treatment peripheral blood samples were obtained from advanced melanoma patients undergoing ICI therapy as monotherapy or in combination at two tertiary care hospitals in Western Australia. Serum VEGF levels were correlated with response to therapy and survival outcomes.Results: Serum VEGF samples were collected from a total of 130 patients treated with ICI therapy (pembrolizumab 73, ipilimumab 15, and ipilimumab/nivolumab combination 42). Median serum VEGF level was significantly higher in the non-responders (82.15 pg/mL) vs. responders (60.40 pg/mL) in the ipilimumab monotherapy cohort (P Conclusions: The results of our study confirm previous
Can serial monitoring of serum Vascular Endothelial Growth Factor (VEGF), Nitric Oxide (NO), and Angiotensin II (ANGII) levels have predictive role during Bevacizumab treatment? - Add Comment #889945
TY - JOUR. T1 - Role of copper and vascular endothelial growth factor (VEGF) on endometrial angiogenesis. AU - Chianeh, Yousef Rezaei. AU - Rao, Pragna. PY - 2013. Y1 - 2013. N2 - The formation of new blood vessels is the initial step in neovascularisation. The first stage in angiogenesis is the activation of endothelial cells. Copper ions stimulate proliferation and immigration of endothelial cells. It has been shown that serum copper concentration increases as the cancer disease progresses and correlates with tumour incidence and burden. Copper ions also activate several proangiogenic factors, e.g., vascular endothelial growth factor, basic fibroblast growth factor, and interleukin 1. This review concerns a brief introduction into the basics of blood vessel development as well as the regulatory mechanisms of this process. The role of copper ions in angiogenesis is discussed.. AB - The formation of new blood vessels is the initial step in neovascularisation. The first stage in angiogenesis is ...
Title: Vascular Endothelial Growth Factor (VEGF) in the Pathogenesis of Diabetic Nephropathy of Type 1 Diabetes Mellitus. VOLUME: 12 ISSUE: 1. Author(s):Maria Mironidou-Tzouveleki, Stergios Tsartsalis and Constantinos Tomos. Affiliation:A Laboratory of Pharmacology, Medical School, Aristotle University of Thessaloniki, Komninon 4, 57010, Filyro, Greece.. Keywords:Nephropathy, pathogenesis, type 1 diabetes mellitus, VEGF, Diabetic nephropathy, Vascular endothelial growth factor, VEGFRs, hypertrophy, PlGF, angiogenesis, Rac, sFlt-1, glomerular endotheliosis, proteinuria, hypertension, glomerulosclerosis, glomerular filtration rate (GFR), Denys-Drash syndrome, nephritic syndrome, renal hypoxia, HIF, ERK, ROS, AGEs, albuminuria, microalbuminuria, CTAD, ELISA, Ranibizumab, Pegaptanib, Aflibercept, VEGF Trap-Eye, angiotensin converting enzyme (ACE). Abstract: Diabetic nephropathy (DN) is a common complication of diabetes mellitus and is the primary cause of endstage renal disease in the Western ...
Angiogenesis, the growth of blood vessel from the existing vasculature, depends on the expression of various growth factors but Vascular Endothelial Growth factor (VEGF) ranks as the key inducer and the central mediator that promotes vascular permeability.
Vascular endothelial growth factor (VEGF) inhibitor medications such as ranibizumab pegaptanib and bevacizumab are in use for the treatment of neovascular age-related macular degeneration (AMD) and additional retinal conditions although only ranibizumab and pegaptanib are authorized for these conditions. instances individuals should be fully knowledgeable concerning their treatment and 20-Hydroxyecdysone any potential risks involved. Off-label drug use can be an important tool to provide individuals with treatment in instances of unmet medical need. However 20-Hydroxyecdysone the use of an unlicensed medicinal product when a appropriate licensed alternative is definitely available puts prescribing physicians at risk of liability if security issues arise. Growing medical evidence suggests security variations exist between ranibizumab and bevacizumab. expression system [6]. Ranibizumab was designed specifically for intravitreal use and in addition to AMD is definitely approved for the treatment of ...
Heroult M., Bernard-Pierrot I., Delbe J., Hamma-Kourbali Y., Katsoris P., Barritault D., Papadimitriou E., Plouet J., Courty J.. Heparin affin regulatory peptide (HARP) is an heparin-binding molecule involved in the regulation of cell proliferation and differentiation. Here, we report that HARP inhibited the biological activity induced by the 165-amino-acid form of vascular endothelial growth factor (VEGF165) on human umbilical vein endothelial cells. Endothelial-cell proliferation induced by VEGF165 showed about 50% inhibition in the presence of HARP in a concentration of 3 nM. In similar range of concentrations, HARP blocked tube formation induced by VEGF165 in three-dimensional angiogenesis assay. In vivo studies showed that HARP inhibited the VEGF165-induced Matrigel trade mark infiltration of endothelial cells. We then investigated the mechanisms of this inhibition and shown that HARP inhibited the binding of 125I-VEGF165 to the VEGF receptors of endothelial cells. Additional studies using ...
Vascular endothelial growth factor (VEGF) is definitely 1 of the many essential angiogenic growth factors for tumor angiogenesis. growth angiogenesis in MMP-2 suppressed growth areas was associated with decreased co-localization of MMP-2 and integrin-V3. In overview, these data offer fresh information into the systems root MMP-2-mediated VEGF appearance in lung growth angiogenesis. and versions. Our results reveal that MMP-2 transcriptional inactivation decreased integrin-V3-mediated considerably, PI3E/AKT-induced VEGF appearance, which reduced tumor cell-induced angiogenesis ultimately. Components AND Strategies Cells and Reagents A549 and L1299 lung adenocarcinoma cells had been cultured in RPMI 1640 (ATCC Manassas, Veterans administration) supplemented with 10% fetal bovine serum (Invitrogen, Carlsbad, California), 50 devices/mL penicillin, and 50 g/mL streptomycin (Existence Systems, Inc., Frederick, MD). For human being microvascular skin endothelial cells (HMEC-1), glutamine, EGF buy ...
Background: Pharmacological inhibitors of vascular endothelial growth factor (VEGF) receptors, like vatalanib, have already been analyzed in randomised trials (CONFIRM (Colorectal Dental Book therapy For the Inhibition of Angiogenesis and Retarding of Metastases) 1 and 2) in colorectal cancer showing activity inside a subgroup of individuals with high serum LDH expression. the placebo group was mentioned (response prices (RRs) 15% (3/20) when high VD 52% (26/50) when low VD; 39 and 40 31, respectively). Therefore, evaluation was performed in mixed CONFIRM 1 and 2 data models, no split analysis 781649-09-0 was attempted due to the low amount of cells collected relatively. So that they can investigate the association of PTZK/ZK restorative activity with tumour angiogenesis and anaerobic metabolic pathways, 781649-09-0 paraffin-embedded materials from 164 individuals with metastatic colorectal adenocarcinoma had been recruited within the CONFIRM 1 and 2 tests. This group of individuals continues to ...
This study will look for the presence in blood of a substance called vascular endothelial growth factor (VEGF) in patients with uveitis (eye inflammation). It will also look for this substance in eye fluid samples taken from patients with uveitis who are undergoing eye surgery.. Some patients with uveitis experience some vision loss during an inflammatory attack because of swelling (edema) in a particular area of the retina called the macula, which is involved in visual acuity. It may be that VEGF is involved in the development of macular edema.. Patients with uveitis who participate in this study will have about 10 cc (2 teaspoons) of blood drawn to be examined for VEGF. They will also undergo a procedure called fluorescein angiography to look at the blood vessels of the eye. A dye called sodium fluorescein is injected into the blood stream through a vein. After the dye reaches the blood vessels of the eye, photographs are taken of the retina.. In addition, patients with uveitis who are ...
Yasuhara, T., Shingo, T., Kobayashi, K., Takeuchi, A., Yano, A., Muraoka, K., Matsui, T., Miyoshi, Y., Hamada, H. and Date, I. (2004), Neuroprotective effects of vascular endothelial growth factor (VEGF) upon dopaminergic neurons in a rat model of Parkinsons disease. European Journal of Neuroscience, 19: 1494-1504. doi: 10.1111/j.1460-9568.2004.03254.x ...
TY - JOUR. T1 - Serum ischemia modified albumin and vascular endothelial growth factor levels following intravitreal bevacizumab injections. AU - Soiberman, Uri. AU - Levy, Ran. AU - Schwartz, Shulamit. AU - Goldstein, Michaella. AU - Loewenstein, Anat. AU - Barak, Adiel. PY - 2013/12/6. Y1 - 2013/12/6. N2 - Purpose: Previous reports have demonstrated that the serum levels of vascular endothelial growth factor (VEGF) are reduced after intravitreal injections of bevacizumab. This study aimed to determine the serum levels of ischemia-modified albumin (IMA), a marker of ischemia, and VEGF following intravitreal injections of bevacizumab. Methods: This was a prospective study. Blood samples were drawn prior to injection and at 1, 7, and 30 days after injection. Results: A total of 11 patients participated in this study. Mean serum IMA levels were lower than baseline during follow-up, with statistically significant differences compared to baseline levels at day 1 and day 30 (preinjection: 49.82 ± ...
Prognostic significance of plasma vascular endothelial growth factor levels in patients with hormone-refractory prostate cancer treated on Cancer and Leukemia Group B 9480.
TY - JOUR. T1 - Anthrax lethal toxin inhibits growth of and vascular endothelial growth factor release from endothelial cells expressing the human herpes virus 8 viral G protein-coupled receptor. AU - Depeille, Philippe. AU - Young, John J.. AU - Boguslawski, Elissa A.. AU - Berghuis, Bree D.. AU - Kort, Eric J.. AU - Resau, James H.. AU - Frankel, Arthur E.. AU - Duesbery, Nicholas S.. PY - 2007/10/1. Y1 - 2007/10/1. N2 - Purpose: In this study, we tested the hypothesis that inhibition of mitogen-activated protein kinase kinases (MKK) inhibits tumor growth by acting on angiogenic signaling and by extension may form the basis of an effective strategy for treatment of Kaposis sarcoma. Experimental Design: Murine endothelial cells expressing the human herpes virus 8 G protein-coupled receptor (vGPCR-SVEC) were treated with anthrax lethal toxin (LeTx). LeTx is a binary toxin ordinarily secreted by Bacillus anthracis and is composed of two proteins: protective antigen (the binding moiety) and ...
KEY POINTS: Combining nitric oxide (NO)-mediated increased blood flow with angiopoietin-1-Tie2 receptor signalling induces arteriolargenesis - the formation of arterioles from capillaries - in a model of physiological angiogenesis. This NO-Tie-mediated arteriolargenesis requires endogenous vascular endothelial growth factor (VEGF) signalling. Inhibition of VEGF signalling increases pericyte coverage in microvessels. Together these findings indicate that generation of functional neovasculature requires close titration of NO-Tie2 signalling and localized VEGF induction, suggesting that the use of exogenous VEGF expression as a therapeutic for neovascularization may not be successful. ABSTRACT: Signalling through vascular endothelial growth factor (VEGF) receptors and the tyrosine kinase with IgG and EGF domains-2 (Tie2) receptor by angiopoietins is required in combination with blood flow for the formation of a functional vascular network. We tested the hypothesis that VEGF and angiopoietin-1 (Ang1)
Title:Targeting Vascular Endothelial Growth Factor in Neuroblastoma. VOLUME: 2 ISSUE: 1. Author(s):Danielle Hsu, Jason M. Shohet and Eugene S. Kim. Affiliation:Division of Pediatric Surgery, Texas Childrens Hospital, CCC Building, Suite 1210, 6701 Fannin St, Houston, TX 77030, USA.. Keywords:Vascular endothelial growth factor, angiogenesis, clinical trials, neuroblastoma.. Abstract:Angiogenesis is critical to tumor growth and metastasis and is dependent on growth factors, such as vascular endothelial growth factor (VEGF). The most characterized angiogenic factor, VEGF is an endothelial cell mitogen and permeability factor that has been found to be overexpressed in almost all human cancers. In a number of tumor model systems, antagonism of the VEGF pathway results in inhibition of angiogenesis and tumor growth. Specifically, VEGF inhibition has been shown to suppress tumor growth, decrease microvasculature, and induce apoptosis of endothelial cells. This close relationship between hypoxia, ...
Angiogenesis, the formation of blood vessels, is essential for preparing a closed circulatory system in the body, and for supplying oxygen and nutrition to tissues. Major diseases such as cancer, rheumatoid arthritis, and atherosclerosis include pathological angiogenesis in their malignant processes, suggesting anti-angiogenic therapy to be a new strategy for suppression of diseases. However, until the 1970s, the molecular basis of angiogenesis was largely unknown. In recent decades, extensive studies have revealed a variety of angiogenic factors and their receptors, including vascular endothelial growth factor (VEGF)-VEGFRs, Angiopoietin-Tie, Ephrin-EphRs and Delta-Notch to be the major regulators of angiogenesis in vertebrates. VEGF and its receptors play a central role in physiological as well as pathological angiogenesis, and functional inhibitors of VEGF and VEGFRs such as anti-VEGF neutralizing antibody and small molecules that block the tyrosine kinase activity of VEGFRs have recently been
In recent years, vascular inflammation, marked by activated monocytes and endothelium, has been proven to play a significant role in the pathogenesis of vasoocclusive events (VOEs) in sickle cell disease (SCD). Vascular endothelial growth factor ( VEGF), an endothelial cell mitogen, has been shown to contribute to the increased endothelial cell adhesivity by increasing the expression of cell adhesion molecules ICAM-1 ( intercellular adhesion molecule-1) and VCAM-1 ( vascular cell adhesion molecule-1) on the endothelium. We have investigated VEGF alterations in 37 patients with SCD during VOEs and/or steady state. VEGF levels ( mean +/- SEM) were found to be significantly elevated during VOEs ( 703.1 +/- 119.0 pg/ml) when compared with those at steady state (258.0 +/- 57.8 pg/ml) and healthy controls (196.6 +/- 21.9 pg/ml) ( p< 0.001). However, we did not find a difference between VEGF concentrations in sickle patients at steady state and the normal subjects ( p> 0.05). We suggest that ...
TY - JOUR. T1 - Vascular endothelial growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats. AU - Cha, Dae-Ryong. AU - Kang, Young Sun. AU - Han, Sang Youb. AU - Jee, Yi Hwa. AU - Han, Kum Hyun. AU - Han, Jee Young. AU - Kim, Young Sik. AU - Kim, Nan Hee. PY - 2004/10/1. Y1 - 2004/10/1. N2 - Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of diabetic nephropathy. We investigated serial changes of VEGF in the kidney and assessed whether glomerular and urinary VEGF levels are related to the severity of diabetic nephropathy. Furthermore, we examined the relationship between urinary VEGF levels and the urinary albumin excretion (UAE) rate in Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats. Glomerular VEGF mRNA expression and protein synthesis were evaluated by the reverse transcription-polymerase chain reaction, immunohistochemical staining and in situ hybridization. Urinary levels of VEGF were determined by enzyme-linked ...
TY - CHAP. T1 - The role of vascular endothelial growth factor in major depression. AU - Lee, Bun Hee. AU - Kim, Yong Ku. PY - 2013. Y1 - 2013. N2 - Vascular endothelial growth factor (VEGF) is a potent angiogenic factor under physiological and pathological conditions, including tumor angiogenesis. Recently, the effects of VEGF on neurons have been reported. VEGF and its high-affinity tyrosine kinase receptors, VEGFR1 and VEGFR2, are expressed in specific brain regions. In addition, VEGF has been suggested to play an important role in the cross-talk between endothelial cells and neuronal progenitors in the hippocampus, indicating that VEGF may stimulate hippocampal neurogenesis. Neurotrophic factors and neurogenesis are associated with the development of major depression and play essential roles in mediating the therapeutic response to antidepressants. Several animal studies have shown that chronic stress decreased the expression of VEGF and VEGFR2 in granular cells. There is also evidence ...
Vascular endothelial growth factor (VEGF) is a potent vascular permeability factor and a mediator of brain edema. To assess the role of vascular endothelial growth factor in eosinophilic meningitis, vascular endothelial growth factor was measured in the cerebrospinal fluid (CSF) and blood of 9 patients with eosinophilic meningitis in a cohort study. VEGFCSF was detected in 8 (90%) of 9 eosinophilic meningitis patients (range, 45-2190 pg/mL) at presentation. The mean VEGFCSF at presentation, 1 week, and 2 weeks after admission was 568 pg/mL, 751 pg/mL, and 1031 pg/mL, respectively. There was an association between VEGFCSF, CSF protein, white cell count, and eosinophil counts. The VEGFSERUM fluctuated during the 6-month follow-up period. These results indicate that vascular endothelial growth factor may be associated with blood-brain barrier disruption in patients with eosinophilic meningitis.
Vitreous levels of vascular endothelial growth factor in eyes with anterior hyaloidal fibrovascular proliferation Takaki Kobayashi, Shigeki Machida, Takamitsu Fujiwara, Tadashi Ishibe, Daijiro KurosakaDepartment of Ophthalmology, Iwate Medical University School of Medicine, Iwate, JapanPurpose: To determine the intravitreal levels of vascular endothelial growth factor (VEGF) in eyes with anterior hyaloidal fibrovascular proliferation (AHFVP).Methods: Three eyes of three patients who underwent vitrectomy for proliferative diabetic retinopathy (PDR) and subsequently developed an AHFVP (AHFVP group) were studied. We measured the level of VEGF in vitreous samples collected at the primary and following operations by enzyme-linked immunosorbent assay. The vitreous levels of VEGF in 25 eyes of 22 patients with PDR were also studied as controls (PDR group).Results: The averaged VEGF level in the samples collected at the primary surgery was 1.98 ± 2.23 ng/mL in the PDR group, and it was 9.07, 1.94, and 8
Hypoxia is a key regulatory factor in tumour growth, activating angiogenesis, glycolysis and cell migration. It is readily recognized by the intracellular accumulation of hypoxia-inducible factor 1alpha (HIF1alpha) and HIF2alpha. Accumulation of HIF1alpha and HIF2alpha was detected immunohistochemically in a series of 46 nodular malignant melanomas of the skin (epithelioid cell variant), treated with wide local excision. The results were correlated with vascular density (VD) and expression of the angiogenesis-stimulating factors vascular endothelial growth factor (VEGF) and thymidine phosphorylase (TP). Further associations were sought with patient prognosis and the important histopathological features of Breslows thickness, Clarks level of invasion, mitotic rate, inflammatory cell infiltrates and tumour ulceration. HIF1alpha and HIF2alpha accumulation in malignant melanomas was directly correlated with VEGF expression. Tumours with high VEGF or HIF2alpha expression were associated with a poorer
TY - JOUR. T1 - Vascular endothelial growth factor regulates excitatory synaptic transmission in hippocampal neurons. AU - Huang, Yu Fei. AU - Yang, Chih Hao. AU - Chiou, Chiuan Shiou. AU - Huang, Chiung Chun. AU - Hsu, Kuei Sen. PY - 2010. Y1 - 2010. N2 - Vascular endothelial growth factor (VEGF), in addition to its essential role in the processes of vascularization and angiogenesis, exerts direct effects on neural cells in the central nervous system. There is abundant evidence indicating that VEGF protects neurons against cell death induced by a variety of insults, including hypoxia/ischemia and seizures. Recent work has demonstrated the expression of VEGF and its receptors in neurons and has revealed that VEGF can act as a neurotrophic factor to regulate neurogenesis and mediate the effects of enriched environment and antidepressants on hippocampal plasticity. Current studies from our laboratory and those of others have found that VEGF can activate divergent signaling components to regulate ...
TY - JOUR. T1 - A Molecular Mechanism Regulating Circadian Expression of Vascular Endothelial Growth Factor in Tumor Cells. AU - Koyanagi, Satoru. AU - Kuramoto, Yukako. AU - Nakagawa, Hiroo. AU - Aramaki, Hironori. AU - Ohdo, Shigehiro. AU - Soeda, Shinji. AU - Shimeno, Hiroshi. PY - 2003/11/1. Y1 - 2003/11/1. N2 - Because angiogenesis is essential for tumor growth and metastasis, inhibition of angiogenesis has emerged as a new therapy to treat cancers. Hypoxia-induced expression of vascular endothelial growth factor (VEGF) plays a central role in tumor-induced angiogenesis. In this study, we found that expression of VEGF in hypoxic tumor cells was affected by the circadian organization of molecular clockwork. The core circadian oscillator is composed of an autoregulatory transcription-translation feedback loop in which CLOCK and BMALL are positive regulators, and Period and Cryptochrome genes act as negative ones. The levels of VEGF mRNA in tumor cells implanted in mice rose substantially in ...
TY - JOUR. T1 - Vascular endothelial growth factor regulation of Weibel-Palade-body exocytosis. AU - Matsushita, Kenji. AU - Yamakuchi, Munekazu. AU - Morrell, Craig N.. AU - Ozaki, Michitaka. AU - ORourke, Brian. AU - Irani, Kaikobad. AU - Lowenstein, Charles J.. PY - 2005/1/1. Y1 - 2005/1/1. N2 - Vascular endothelial growth factor (VEGF) not only regulates angiogenesis, vascular permeability, and vasodilation but also promotes vascular inflammation. However, the molecular basis for the proinflammatory effects of VEGF is not understood. We now show that VEGF activates endothelial cell exocytosis of Weibel-Palade bodies, releasing vasoactive substances capable of causing vascular thrombosis and inflammation. VEGF triggers endothelial exocytosis in part through calcium and phospholipase C-γ (PLC-γ) signal transduction. However, VEGF also modulates endothelial cell exocytosis by activating endothelial nitric oxide synthase (eNOS) production of nitric oxide (NO), which nitrosylates ...
TY - JOUR. T1 - Vascular endothelial growth factor as a biomarker for the early detection of cancer using a whole cell-based biosensor. AU - May, Kimberly M L. AU - Vogt, Adam. AU - Bachas, Leonidas G. AU - Anderson, Kimberly W.. PY - 2005/6. Y1 - 2005/6. N2 - Vascular endothelial growth factor (VEGF) is a cytokine and endothelial cell (EC) mitogen that has been studied for its role in angiogenesis of malignant tumors. Elevated quantities of VEGF in the serum and plasma of patients have been correlated with the presence of cancer and metastasis. Since VEGF induces hyperpermeability of EC monolayers, this protein can be detected in vitro with a whole cell-based biosensor. This biosensor consists of a confluent monolayer of human umbilical vein endothelial cells (HUVECs) attached to a cellulose triacetate (CTA) membrane of an ion-selective electrode (ISE). Previous studies regarding this biosensor have shown that when the biosensor was exposed to a model toxin, such as histamine, the response of ...
Up-regulation of vascular endothelial growth factor (VEGF) expression is a major event leading to neovascularization in malignant gliomas. Hypoxia is believed to be the crucial environmental stimulus for this up-regulation. To critically assess this hypothesis, we asked whether the mechanisms defined previously for hypoxia-induced VEGF expression in vitro are similarly involved and sufficient for up-regulation of VEGF gene expression in vivo, using a lacZ reporter gene under the control of VEGF regulatory sequences in an experimental glioma model. Inclusion of the binding site for hypoxia-inducible factor 1 (HIF 1) in the 5′ regulatory sequences used in the hybrid gene produced weak β-galactosidase staining in a special tumor cell subtype, the so-called perinecrotic palisading (PNP) cells that flank necrotic regions within the tumor. Deletion of the HIF 1 binding site abolished reporter gene expression in the PNP cells, indicating that transcriptional activation of VEGF expression in gliomas ...
Vascular Endothelial Growth Factor from mouse (mVEGF ); VEGF, E. coli, powder, cell culture; Suitable for mammalian cell culture; Vascular endothelial growth factor (VEGF) supports development of new blood vessels during embryonic development and after vascular injury; Vascular endothelial gr
TY - JOUR. T1 - Targeting Bacteroides in Stool Microbiome and Response to Treatment With First-Line VEGF Tyrosine Kinase Inhibitors in Metastatic Renal-Cell Carcinoma. AU - Hahn, Andrew W.. AU - Froerer, Camryn. AU - VanAlstine, Sidney. AU - Rathi, Nityam. AU - Bailey, Erin B.. AU - Stenehjem, David D.. AU - Agarwal, Neeraj. PY - 2018/10. Y1 - 2018/10. N2 - Vascular endothelial growth factor (VEGF) tyrosine kinase inhibitors (TKI) are a mainstay of treatment for metastatic renal-cell carcinoma. Stool microbiome composition is predictive of response to immunotherapy and cytotoxic chemotherapy. Antibiotics targeting Bacteroides species are associated with improved progression-free survival while receiving first-line VEGF-TKIs. Background: Vascular endothelial growth factor (VEGF) tyrosine kinase inhibitors (TKIs) are a mainstay of treatment for metastatic renal-cell carcinoma. Stool microbiome composition is predictive of response to immunotherapy and cytotoxic chemotherapy. We sought to ...
TY - JOUR. T1 - Increased vascular endothelial growth factor transcription in residual hepatocellular carcinoma after open versus laparoscopic hepatectomy in a small animal model. AU - Perry, Kyle A.. AU - Enestvedt, Charles. AU - Hosack, Luke W.. AU - Pham, Thai H.. AU - Diggs, Brian S.. AU - Teh, Swee. AU - Orloff, Susan. AU - Winn, Shelly. AU - Hunter, John. AU - Sheppard, Brett. PY - 2010/5. Y1 - 2010/5. N2 - Background Vascular endothelial growth factor (VEGF) is overexpressed in hepatocellular carcinoma (HCC), and findings have shown that its upregulation in these tumors has an impact on tumor growth. The authors hypothesized that compared with open liver resection, laparoscopic hepatectomy would result in a decreased local angiogenic response in residual tumor cells. Methods Right- and left-lobe hepatomas were induced in Buffalo rats via laparoscopically guided subcapsular injection of Morris hepatoma cells. After 1 week, the animals were randomized to laparoscopic or open left lateral ...
Vascular endothelial growth factor (VEGF) gene is highly polymorphic, and single nucleotide polymorphisms (SNP) of VEGF gene are associate with cancer prognosis. This study aimed to analyze the correlation of VEGF gene polymorphisms with grade and prognosis of lung cancer. A total of 458 Chinese patients with primary lung cancer were enrolled from September 2008 to October 2013. The genotypes of −2578C | A, −1154G | A, − 460 T | C, and + 405G | C were analyzed in white blood cells from patients using polymerase chain reaction based restriction fragment length polymorphism. Our data showed that -1154G | A polymorphism was significantly associated with tumor stages, but all four tested VEGF gene polymorphisms had no significant effect on survival. VEGF polymorphisms may relate to stage of lung cancer in Chinese population.
The purpose of this study is to evaluate the activity of RO4929097 in renal cell carcinoma patients that have failed therapy with VEGF/VEGFR directed ag
TY - JOUR. T1 - Vascular endothelial growth factor induces protein synthesis in renal epithelial cells. T2 - A potential role in diabetic nephropathy. AU - Senthil, Duraisamy. AU - Choudhury, Goutam Ghosh. AU - McLaurin, Colby. AU - Kasinath, Balakuntalam S.. N1 - Funding Information: We thank Dr. D.J. Riley for helping with induction of diabetes and critical reading of the manuscript and Dr. N. Sonenberg, K. Walsh, for mutant constructs employed in this study. This study was supported by funding from the American Diabetes Association (B.S.K.), Veterans Administration Research Service (Merit and REAP awards for B.S.K. and G.G.C.), the National Institutes of Health (G.G.C. DK55815), and the National Kidney Foundation of South and Central Texas (D.S.).. PY - 2003/8/1. Y1 - 2003/8/1. N2 - Background. Vascular endothelial growth factor (VEGF) is an important determinant of ocular complications of diabetes. Its potential role in diabetic renal disease has not been extensively studied. Methods. We ...
98. Fraenzer, J.-Th., Wachs, F.P., Licht, K., Gleich, O., Strutz, J. (2006) Charakterisierung von Vascular Endothelial Growth Factor (VEGF) und seines Rezeptors Flk-1 in Zellkulturen aus dem Innenohr neugeborener Mäuse. 9. Jahrestagung der Deutschen Gesellschaft für Audiologie. p139. 99. Fraenzer, J.-Th., Wachs, F.P., Licht, K., Gleich, O., Strutz, J. (2006) Charakterisierung von Vascular Endothelial Growth Factor (VEGF) und seines Rezeptors Flk-1 in Zellkulturen aus dem Innenohr neugeborener Mäuse. Vortragskurzfassung 9. Jahrestagung der Deutschen Gesellschaft für Audiologie, Tagungs-CD ISBN 3-9809869-5-0. 100. Gleich, O., Fraenzer, J.-Th., Strutz, J., (2007) Preliminary data evaluating the effect of Gabapentin on auditory temporal resolution characterized by a gap detection task in gerbils. Abstr. 30th ARO Midwinter Res. Mtg. 316-317. 101. Gleich, O., Thurnbauer, K., Strutz, J., (2007) Differentielle altersbedingte Veränderungen in den Unterkernen des Nucleus cochlearis der ...
Edman degradation analyses and co-migration of synthetic peptides with EGFR-derived tryptic phosphopeptides identify these sites as Tyr845 and Tyr1101. Equilibrium population dynamics when mating is by mutual choice based on age. The silver grains do not 100mg viagra without a doctor prescription appear localized at postsynaptic level. The patient was discharged from hospital 18 days after treatment with NIHSS score 5. Maximal endothelial tissue plasminogen activator release is not impaired in patients with acute coronary syndromes before heparin treatment.. Temporal sequence of cell wall disassembly events in generic cialis developing fruits. Elderly trauma in a resource-poor area in sub-Saharan Africa is associated with a significant increase in hospital admissions and mortality. Other environmental changes may be needed to facilitate more thorough support. The directional transport of the phytohormone auxin represents a key, plant-specific mechanism for polarization and patterning in complex ...
Over-expression of truncated epidermal growth factor receptor (EGFR) occurs in a variety of malignancies including glioblastoma multiforme, breast and lung cancer. The truncation deletes an extracellular domain and results in constitutive activation of the receptor. NIH3T3 cells were transfected with full length or truncated human EGFR and differences in growth rates in vivo and in vitro analysed. A growth advantage was seen for cells expressing mutant receptor compared to full length EGFR in vivo only. Administration of an anti-mutant EGFR antibody to mice transiently reduced the growth rates of mutant tumours, confirming that the mutant receptor itself was important in this enhanced tumorigenicity. This showed that stimuli present in vivo and not in vitro may be contributing to growth. We therefore analysed the regulation of the angiogenic factor vascular endothelial growth factor (VEGF). Although levels of secreted VEGF did not differ significantly between wild-type and mutant EGFR cell lines when
Vascular endothelial growth factor (VEGF) functions as a regulator of neovascularization in malignant cells. VEGF as a mitogen is thought to alter renal cell carcinoma formation and tumor progression. We investigated the expression of the VEGF gene in order to evaluate its clinical significance in renal cell carcinoma. Tissue samples from 198 patients with renal cell carcinoma were examined with an immunohistochemical stain for the expression of the VEGF gene. The expression rate was compared to 34 normal renal cortical samples obtained from renal surgery from noncancer patients. There were significant differences between normal renal cortex (0%) and cancer tissue (54.5%) in positive staining of VEGF protein (P|0.001). With the progression of tumor grade, the positive rate of VEGF gene expression significantly increased. The expression rate of the VEGF gene in the advanced group, such as with lymph node involvement or vein invasion, was greater than that in the locally confined group (P|0.001). The
Previous work showed that connexin 43 (Cx43) reduced the expression of hypoxic-induced factor-1α (HIF-1α) in astrocytes. HIF-1α is a master transcription factor for angiogenesis in tumor. Angiogenesis is essential for tumor progression. Here, we investigated the role of Cx43 in vascular endothelial growth factor (VEGF) production and angiogenesis in murine tumor. In the study, mouse B16F10 and 4T1 cells were overexpressed or knockdown with Cx43. The expression profiles as well as activity of the treated cells were examined. Furthermore, reduced Cx43 expression in B16F10 and 4T1 cells causes increased expression of VEGF and enhanced the proliferation of endothelial cells. On the contrary, the expression of VEGF and the proliferation of endothelial were increased in the conditioned medium of Cx43-knockdown tumor cells. We subcutaneously transplanted Cx43-overexpressing B16F10 cells into mice to evaluate the roles of Cx43 in the tumor angiogenesis. Both tumor size and the number of vessels growing in
Tubulin-binding vascular-disrupting agents (VDA) are currently in clinical trials for cancer therapy but the factors that influence tumor susceptibility to these agents are poorly understood. We evaluated the consequences of modifying tumor vascular morphology and function on vascular and therapeutic response to combretastatin-A4 3-O-phosphate (CA-4-P), which was chosen as a model VDA. Mouse fibrosarcoma cell lines that are capable of expressing all vascular endothelial growth factor (VEGF) isoforms (control) or only single isoforms of VEGF (VEGF120, VEGF164, or VEGF188) were developed under endogenous VEGF promoter control. Once tumors were established, VEGF isoform expression did not affect growth or blood flow rate. However, VEGF188 was uniquely associated with tumor vascular maturity, resistance to hemorrhage, and resistance to CA-4-P. Pericyte staining was much greater in VEGF188 and control tumors than in VEGF120 and VEGF164 tumors. Vascular volume was highest in VEGF120 and control tumors ...
1. Klein R, Peto T, Bird A, Vannewkirk MR. The epidemiology of age-related macular degeneration. American journal of ophthalmology. 2004;137:486-95 2. Ambati J, Ambati BK, Yoo SH, Ianchulev S, Adamis AP. Age-related macular degeneration: etiology, pathogenesis, and therapeutic strategies. Survey of ophthalmology. 2003;48:257-93 3. van Wijngaarden P, Qureshi SH. Inhibitors of vascular endothelial growth factor (VEGF) in the management of neovascular age-related macular degeneration: a review of current practice. Clin Exp Optom. 2008;91:427-37 4. Ferrara N. Vascular endothelial growth factor and age-related macular degeneration: from basic science to therapy. Nat Med. 2010;16:1107-11 5. Kovach JL, Schwartz SG, Flynn HW Jr, Scott IU. Anti-VEGF Treatment Strategies for Wet AMD. J Ophthalmol. 2012;2012:786870 6. Ferrara N, Adamis AP. Ten years of anti-vascular endothelial growth factor therapy. Nat Rev Drug Discov. 2016;15:385-403 7. Park YG, Rhu HW, Kang S, Roh YJ. New Approach of Anti-VEGF Agents ...
The original member of the family of endothelial cell growth factors referred to as VASCULAR ENDOTHELIAL GROWTH FACTORS. Vascular endothelial growth factor-A was originally isolated from tumor cells and referred to as tumor angiogenesis factor and vascular permeability factor. Although expressed at high levels in certain tumor-derived cells it is produced by a wide variety of cell types. In addition to stimulating vascular growth and vascular permeability it may play a role in stimulating VASODILATION via NITRIC OXIDE-dependent pathways. Alternative splicing of the mRNA for vascular endothelial growth factor A results in several isoforms of the protein being produced ...
Angiogenesis is essential in physiological processes including ovulation, implantation and pregnancy. One of the most potent regulators is the cytokine vascular endothelial growth factor (VEGF). We provide evidence for a novel pregnancy-associated soluble variant of the VEGF receptor Flt-1. VEGF ranged from undetectable to 157.3 pg/ml (mean 49.9 pg/ml, SD 48.4 pg/ml) in plasma samples from normal volunteers (n = 10), but was undetectable in plasma from pregnant women (n = 12) and amniotic fluid (n = 10). Recoveries of spiked VEGF were poor in pregnancy-related samples, indicating the presence of VEGF-binding activity which was confirmed using biosensor and chromatographic techniques. Partial purification and protein sequencing indicated a novel soluble form of Flt-1 with a subunit size of 150 kDa. Normally present as a multimeric structure of approximately 400-550 kDa, complexes of 600-700 kDa were formed following binding of multiple VEGF molecules. Reverse transcriptase polymerase chain ...
Purpose This study was aimed to identify the expression pattern of vascular endothelial growth factor (VEGF) in non-small cell lung cancer (NSCLC) and to explore its potential correlation with the progression of NSCLC. Methods Gene expression profile GSE39345 was downloaded from the Gene Expression Omnibus database. Twenty healthy controls and 32 NSCLC samples before chemotherapy were analyzed to identify the differentially expressed genes (DEGs). Then pathway enrichment analysis of the DEGs was performed and protein-protein interaction networks were constructed. Particularly, VEGF genes and the VEGF signaling pathway were analyzed. The sub-network was constructed followed by functional enrichment analysis. Results Total 1666 up-regulated and 1542 down-regulated DEGs were identified. The down-regulated DEGs were mainly enriched in the pathways associated with cancer. VEGFA and VEGFB were found to be the initiating factor of VEGF signaling pathway. In addition, in the epidermal growth factor receptor
The induction by hypoxia of genes such as erythropoietin, vascular endothelial growth factor (VEGF), and glucose transporter-1 (Glut-1) is mediated in part by a transcriptional complex termed hypoxia-inducible factor-1 (HIF-1). Several lines of evidence have implicated protein phosphorylation in the mechanism of activation of HIF-1 by hypoxia. Recent reports have described the activation of the tyrosine kinase src by severe hypoxia, and a role in the induction of VEGF by severe hypoxia has been proposed. This led us to examine whether src and related kinases operated more widely in the hypoxic induction of HIF-1 and HIF-1-dependent genes regulated by hypoxia. Measurements of src kinase activity in cells exposed to varying severities of hypoxia showed activation by severe hypoxia (0.1% oxygen or catalyst induced anoxia), but not 1% oxygen. This contrasted with the marked induction of HIF-1 by exposure to 1% oxygen. Manipulations of src activity were produced by transient and stable transfection of Hep3B
The growth and metastasis of tumors depend on the development of an adequate blood supply via angiogenesis. Recent studies indicate that the inducible nitric oxide synthase (iNOS), vascular endothelial growth factor (VEGF) and the tumor suppressor p53 are fundamental play-markers of the angiogenic process. Overexpression of iNOS and VEGF has been shown to induce angiogenesis in tumors. P53 suppresses angiogenesis by down-regulating VEGF and iNOS. The correlation of expression of p53, VEGF and iNOS and clinical features in gastric carcinogenesis, however, has not been well characterized. The expression of p53, iNOS and VEGF in gastric precancerous and cancerous lesions and its relation with the clinical features was determined with immunohistochemistry (avidin-biotin-peroxidase complex method) on 55 randomly selected GC patients and 60 symptom-free subjects from the mass survey in the high-incidence area for GC in Henan, northern China. The positive immunostainig rates for p53, iNOS and VEGF in gastric
Steroid Responsive Meningitis-Arteritis (SRMA) is a common cause of inflammation of the canine central nervous system (CNS). To investigate if transforming growth factor beta 1 (TGF-β1), interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) are involved in the production of excessive immunoglobulin A (IgA), the induction of acute phase proteins and in the development of a systemic necrotizing vasculitis, characteristic of SRMA, these three signalling proteins were evaluated. Cerebrospinal fluid (CSF) and serum samples of dogs during the acute phase of SRMA (SRMA) were tested for IL-6, VEGF and TGF- β1. Results were compared to those of dogs affected with SRMA during treatment (SRMA Th) and during relapse (SRMA R), to dogs with other meningoencephalomyelitides (ME), with miscellaneous non-inflammatory diseases of the CNS (CNS-Mix), with idiopathic epilepsy (IE), with systemic inflammatory diseases (Syst. Infl.) and with healthy dogs (Healthy). Concentrations of IL-6 and VEGF in CSF were
Hashimotos thyroiditis is an autoimmune disorder and the most common cause of hypothyroidism. The use of Nigella sativa, a potent herbal medicine, continues to increase worldwide as an alternative treatment of several chronic diseases including hyperlipidemia, hypertension and type 2 diabetes mellitus (T2DM). The aim of the current study was to evaluate the effects of Nigella sativa on thyroid function, serum Vascular Endothelial Growth Factor (VEGF) - 1, Nesfatin-1 and anthropometric features in patients with Hashimotos thyroiditis. Forty patients with Hashimotos thyroiditis, aged between 22 and 50 years old, participated in the trial and were randomly allocated into two groups of intervention and control receiving powdered Nigella sativa or placebo daily for 8 weeks. Changes in anthropometric variables, dietary intakes, thyroid status, serum VEGF and Nesfatin-1 concentrations after 8 weeks were measured. Treatment with Nigella sativa significantly reduced body weight and body mass index (BMI).
Vascular Endothelial Growth Factor C (Flt4 Ligand or Vascular Endothelial Growth Factor Related Protein or VEGFC) - Drugs in Development, 2021 provides in depth analysis on Vascular Endothelial Growth Factor C (Flt4 Ligand or Vascular Endothelial Growth Factor Related Protein or VEGFC) targeted pipeline therapeutics. The report provides comprehensive information complete with Analysis by Indications, Stage of Development, Mechanism of Action (MoA), Route of Administration (RoA) and Molecule Type. The report also covers the descriptive pharmacological action of the therapeutics, its complete research and development history and latest news and press releases. Additionally, the report provides an overview of key players involved in Vascular Endothelial Growth Factor C (Flt4 Ligand or Vascular Endothelial Growth Factor Related Protein or VEGFC) targeted therapeutics development and features dormant and discontinued projects. The report analyses the pipeline products across relevant therapy areas ...
TY - JOUR. T1 - Lysophosphatidic acid induction of vascular endothelial growth factor expression in human ovarian cancer cells. AU - Hu, Yu Long. AU - Tee, Meng Kian. AU - Goetzl, Edward J.. AU - Auersperg, Nelly. AU - Mills, Gordon B.. AU - Ferrara, Napoleone. AU - Jaffe, Robert B.. N1 - Copyright: Copyright 2020 Elsevier B.V., All rights reserved.. PY - 2001/5/16. Y1 - 2001/5/16. N2 - Background: Lysophosphatidic acid (LPA) stimulates ovarian tumor growth at concentrations present in ascitic fluid. Vascular endothelial growth factor (VEGF) stimulates angiogenesis and plays a pivotal role in the formation of ovarian cancer-associated ascites. We examined whether LPA promotes ovarian tumor growth by increasing angiogenesis via VEGF. Methods: VEGF expression was examined in a simian virus 40 T-antigen-immortalized ovarian surface epithelial cell line (IOSE-29) and in ovarian cancer cell lines (OVCAR-3, SKOV-3, and CAOV-3) treated with LPA. VEGF promoter activity was measured in OVCAR-3 cells ...
TY - JOUR. T1 - Vascular endothelial growth factor expression in pig latissimus dorsi myocutaneous flaps after ischemia reperfusion injury. AU - Erdmann, Detlev. AU - Sweis, Ranya. AU - Wong, Michael S.. AU - Niklason, Laura E.. AU - Du Laney, Tracey V.. AU - Levin, L. Scott. AU - Klitzman, Bruce. AU - Olbrich, Kevin C.. PY - 2003/2/1. Y1 - 2003/2/1. N2 - Exogenous administration of vascular endothelial growth factor (VEGF) improves long-term viability of myocutaneous flaps. However, endogenous expression of this substance in flaps following ischemia-reperfusion injury has not been reported previously. Endogenous production of VEGF was measured in myocutaneous pig latissimus dorsi flaps after ischemia-reperfusion injury. Latissimus dorsi myocutaneous flaps (15 × 10 cm) were simultaneously elevated bilaterally in six Yorkshire-type male pigs (25 kg). Before elevation, three flap zones (5 × 10 cm) were marked according to their distance from the vascular pedicle. After isolation of the vascular ...
Hydrocele is a build-up of fluid in the scrotal regions of a proportion of men infected with the filarial nematode Wuchereria bancrofti. Vascular endothelial growth factors (VEGF) are major mediators of vascular permeability and angiogenesis in the development and progression of many diseases, making them candidates in hydrocele development. We assessed the role of VEGF-A genetic polymorphisms in hydrocele development in a cohort of lymphatic filariasis patients from Ghana. Three VEGF-A promoter polymorphisms were examined. The C/C genotype at −460 was significantly higher in hydrocele patients ([P = 0.0007], OR = 3.8 [95% CI = 1.9-8.2]) than in non-hydrocele patients. Furthermore, plasma levels of VEGF-A were significantly higher in subjects with the C/C genotype than in those with other genotypes. Also, a positive correlation (R2 = 0.412, P = 0.026) was observed between plasma VEGF-A and stage of hydrocele. The data suggest that the C polymorphism at −460 is a genetic risk factor for hydrocele
TY - JOUR. T1 - Plasma cytokines eotaxin, MIP-1α, MCP-4, and vascular endothelial growth factor in acute lower respiratory tract infection. AU - Relster, Mette Marie. AU - Holm, Anette. AU - Pedersen, Court. N1 - © 2016 APMIS. Published by John Wiley & Sons Ltd.. PY - 2017. Y1 - 2017. N2 - Major overlaps of clinical characteristics and the limitations of conventional diagnostic tests render the initial diagnosis and clinical management of pulmonary disorders difficult. In this pilot study, we analyzed the predictive value of eotaxin, macrophage inflammatory protein 1 alpha (MIP-1α), monocyte chemoattractant protein 4 (MCP-4), and vascular endothelial growth factor (VEGF) in 40 patients hospitalized with acute lower respiratory tract infections (LRTI). The cytokines contribute to the pathogenesis of several inflammatory respiratory diseases, indicating a potential as markers for LRTI. Patients were stratified according to etiology and severity of LRTI, based on baseline C-reactive protein and ...
purpose. To investigate whether triamcinolone acetonide (TA) affects the expression of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF) in retinal pigment epithelial (RPE) cells exposed to oxidative stress.. methods. TA (10 nM, 1 μM, or 100 μM) was added to ARPE19 cells exposed to oxidative stress induced by hypoxia-reoxygenation and paraquat. Cellular expression of VEGF, CTGF, and an inducer of both growth factors, transforming growth factor (TGF)-β was investigated with real-time reverse transcription-polymerase chain reaction and Western blot analysis. Tube-forming assays were conducted with human umbilical vein endothelial cells (HUVECs) in conditioned medium from RPE cells exposed to oxidative stress, with or without TA treatment.. results. Oxidative stress induced mRNA expression of VEGF, CTGF, and TGF-β by RPE cells. TA reduced upregulation of VEGF and TGF-β in a concentration-dependent manner. In contrast, upregulation of CTGF by oxidative stress ...
Introduction== Vascular endothelial growth factor (VEGF) secreted protein growth factor family which stimulates the proliferation of vasular endotheial cells and therefore blood vessel growth. VEGF is secreted but remains associated with cells or extracellular matrix. It is released by heparin. VEGF belongs to the platelet derive growth factor (PDGF) family, has four isoforms are formed by alternative splicing of the same gene. {{Factor Links}} , [[Cardiovascular_System_-_Blood_Vessel_Development,Blood Vessel Development]] , [[:Category:VEGF,Category:VEGF]] == Some Recent Findings == {, ,-bgcolor=F5FAFF , * Visceral Endoderm Expression of Yin-Yang1 (YY1) Is Required for VEGFA Maintenance and Yolk Sac Development,ref name=PMID23554936>,pubmed>23554936,/pubmed>,/ref> Mouse embryos lacking the polycomb group gene member Yin-Yang1 (YY1) die during the peri-implantation stage. To assess the post-gastrulation role of YY1, a conditional knock-out (cKO) strategy was used to delete YY1 from ...
Purpose: The study aimed to evaluate and correlate between the levels of vascular endothelial growth factor (VEGF) in serum and aqueous humor in cases of neovascular glaucoma (NVG) to stand up on if it can be used as a marker for early detection of such cases. Methods: This observational case control study included 60 eyes, divided into 3 groups, group A of 30 eyes presented by cataract of different causes (not diabetic patients and no signs of NVG) as a control group and group B of 30 eyes with NVG due to different causes, group C of the same eyes in group B but after one month of treatment by intravitreal bevacizumab and laser treatment by pan retinal photocoagulation (PRP). Serum VEGF was estimated in all groups, also aqueous humor VEGF was estimated in group A and B only. In addition glycosylated hemoglobin (HbA1c) was estimated in group B; statistical analysis of the results was performed. Results: The study revealed that the commonest cause of NVG was proliferative diabetic retinopathy (PDR) in 26
To observe the effect of electro-acupuncture (EA) on tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in peripheral blood and joint synovia in patients with rheumatoid arthritis (RA) to verify the clinical efficacy of E
Kinase insert domain receptor (KDR) is one of two main receptors for vascular endothelial growth factor (VEGF). KDR is a type III receptor tyrosine kinase that is the main mediator of VEGF-induced proliferation, survival, migration, and differentiation in endothelial cells. KDR is also known as fetal liver kinase 1 (Flk1), protein-tyrosine kinase receptor flk-1, vascular endothelial growth factor receptor 2 (VEGFR2), CD309, and tyrosine kinase growth factor receptor. Binding of VEGFA, VEGFC, or VEGFD to KDR initiates several signaling cascades, including pathways that involve protein kinase C (PKC), mitogen-activated protein (MAP) kinases, and AKT1 kinase. Mutations in the KDR gene are associated with infantile capillary hemangiomas.. ...
Kinase insert domain receptor (KDR) is one of two main receptors for vascular endothelial growth factor (VEGF). KDR is a type III receptor tyrosine kinase that is the main mediator of VEGF-induced proliferation, survival, migration, and differentiation in endothelial cells. KDR is also known as fetal liver kinase 1 (Flk1), protein-tyrosine kinase receptor flk-1, vascular endothelial growth factor receptor 2 (VEGFR2), CD309, and tyrosine kinase growth factor receptor. Binding of VEGFA, VEGFC, or VEGFD to KDR initiates several signaling cascades, including pathways that involve protein kinase C (PKC), mitogen-activated protein (MAP) kinases, and AKT1 kinase. Mutations in the KDR gene are associated with infantile capillary hemangiomas.. ...
TY - JOUR. T1 - Arg-leu-tyr-glu suppresses retinal endothelial permeability and choroidal neovascularization by inhibiting the VEGF receptor 2 signaling pathway. AU - Park, Wonjin. AU - Baek, Yi Yong. AU - Kim, Joohwan. AU - Jo, Dong Hyun. AU - Choi, Seunghwan. AU - Kim, Jin Hyoung. AU - Kim, Taesam. AU - Kim, Suji. AU - Park, Minsik. AU - Kim, Ji Yoon. AU - Won, Moo Ho. AU - Ha, Kwon Soo. AU - Kim, Jeong Hun. AU - Kwon, Young Guen. AU - Kim, Young Myeong. PY - 2019/9. Y1 - 2019/9. N2 - Vascular endothelial growth factor (VEGF) plays a pivotal role in pathologic ocular neovascularization and vascular leakage via activation of VEGF receptor 2 (VEGFR2). This study was undertaken to evaluate the therapeutic mechanisms and effects of the tetrapeptide Arg-Leu-Tyr-Glu (RLYE), a VEGFR2 inhibitor, in the development of vascular permeability and choroidal neovascularization (CNV). In cultured human retinal microvascular endothelial cells (HRMECs), treatment with RLYE blocked VEGF-Ainduced phosphorylation ...
The pathogenesis of rheumatoid arthritis (RA) and osteoarthritis (OA) remains obscure, although angiogenesis appears to play an important role. We recently confirmed an overexpression of two angiogenic factors, namely vascular endothelial growth factor (VEGF) and platelet-derived endothelial cell growth factor (PD-ECGF), by the lining and stromal cells of the synovium in both conditions. Because hypoxia inducible factor (HIF)-1α and HIF-2α are essential in regulating transcription of the VEGF gene, active participation of HIF-α molecules in the pathogenesis of these arthritides is anticipated. We investigated the immunohistochemical expression of HIF-1α and HIF-2α in the synovium of 22 patients with RA, 34 patients with OA and 22 normal nonarthritic individuals, in relation to VEGF, VEGF/KDR (kinase insert domain protein receptor) vascular activation, PD-ECGF and bcl-2. A significant cytoplasmic and nuclear overexpression of HIF-1α and HIF-2α was noted in the synovial lining and stromal cells
Purpose : Diabetic Macular Edema (DME) is a vascular endothelial growth factor (VEGF) driven process that can be effectively treated with intravitreal injections of anti-VEGF agents bevacizumab and ranibizumab. In a subset of patients, DME persists and visual loss occurs despite active treatment with these anti-VEGF agents. The Food and Drug Administration recently approved aflibercept, now a third commonly used intravitreous anti-VEGF agent. This retrospective chart review identified patients with persistent DME as nonresponders, and tested the hypothesis that treatment with aflibercept improves functional and structural outcomes in patients that were otherwise resistant to prior anti-VEGF therapies. Methods : The design of this study is a single center, retrospective chart review. Consecutive eyes previously receiving intravitreal bevacizumab (1.25mg) or ranibizumab (0.3mg) for chronic DME and later switched to aflibercept (2mg) were identified. Inclusion criteria included nonresponding ...
Background: Vascular endothelial growth factor (VEGF) inhibitors disrupt angiogenesis and slow tumor growth but have a clinically significant side effect of hypertension. Between 9-59% of patients may develop hypertension induced VEGF inhibitors. Medication labeling for VEGF inhibitors recommend standard pharmacologic treatment of hypertension, interruption of chemotherapy, or discontinuation during hypertensive crisis. Actively controlling patients blood pressure allows them to receive the optimal dose of antineoplastic agent without the complication of hypertension. The purpose of this study is to evaluate an institutions practices of monitoring, identifying, and treating patients VEGF inhibitor induced hypertension. Methods: This retrospective, single-center, chart review assessed patients blood pressure measurements who received bevacizumab, ramucirumab, sorafenib, regorafenib, sunitinib, or pazopanib. Patients were excluded if they were less than 18, received VEGF inhibitors for ...
Vascular endothelial growth factor B also known as VEGF-B is a protein that, in humans, is encoded by the VEGF-B gene. VEGF-B is a growth factor that belongs to the vascular endothelial growth factor family, of which VEGF-A is the best-known member. In contrast to VEGF-A, VEGF-B plays a less pronounced role in the vascular system: Whereas VEGF-A is important for the formation of blood vessels, such as during development or in pathological conditions, VEGF-B seems to play a role only in the maintenance of newly formed blood vessels during pathological conditions. VEGF-B plays also an important role on several types of neurons. It is important for the protection of neurons in the retina and the cerebral cortex during stroke and of motoneurons during motor neuron diseases such as amyotrophic lateral sclerosis. VEGF-B exerts its effects via the FLT1 receptor. VEGF-B has also been found to control endothelial uptake and transport of fatty acids in heart and skeletal muscle. Vascular endothelial ...
Delayed administration of vascular endothelial growth factor (VEGF) promotes functional recovery after focal cerebral ischemia. However, early intravenous injection of VEGF increases blood-brain barrier (BBB) leakage, hemorrhagic transformation and infarct volume whereas its application to cortical surface is neuroprotective. We have investigated whether or not early intracerebroventricular administration of VEGF could replicate the neuroprotective effect observed with topical application and the mechanism of action of this protection. Mice were subjected to 90 mins middle cerebral artery (MCA) occlusion and 24h of reperfusion. Vascular endothelial growth factor (8ng, intracerebroventricular) was administered 1 or 3h after reperfusion. Compared with the vehicle-treated (intracerebroventricular) group, VEGF decreased the infarct volume along with BBB leakage in both treatment groups. Neurologic disability scores improved in parallel to the changes in infarct volume. Independently of the decrease ...
TY - JOUR. T1 - DLC1 negatively regulates angiogenesis in a paracrine fashion. AU - Shih, Yi Ping. AU - Liao, Yi Chun. AU - Lin, Yuan. AU - Lo, Su Hao. PY - 2010/11/1. Y1 - 2010/11/1. N2 - The Rho GTPase-activating protein DLC1 is a tumor suppressor that is often deleted in liver cancer and downregulated in other cancers. DLC1 regulates the actin cytoskeleton, cell shape, adhesion, migration, and proliferation through its Rho GTPase-activating protein activity and focal adhesion localization. In this study, we silenced DLC1 in nonmalignant prostate epithelial cells to explore its tumor suppression functions. Small hairpin RNA-mediated silencing of DLC1 was insufficient to promote more aggressive phenotypes associated with tumor cell growth. In contrast, DLC1 silencing promoted pro-angiogenic responses through vascular endothelial growth factor (VEGF) upregulation, accompanied by the accumulation of hypoxia-inducible factor 1α and its nuclear localization. Notably, modulation of VEGF expression ...
A vascular endothelial growth factor expressed in a variety of tissues. It binds with high specificity to VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-1 and NEUROPILIN-1 ...
The effects of polydeoxyribonucleotide (PDRN), an agonist of the A2A adenosine receptors which when activated positively influences sperm activity, were tested in an experimental testicular ischaemia ⁄ reperfusion injury model. Anaesthetized male Sprague-Dawley rats were subjected to testicular torsion-induced ischaemia, followed by reperfusion (TI ⁄ R). Immediately after detorsion, randomized animals, including SHAM, received intraperitoneal injections of: (i)vehicle (1 mL⁄ kg 0.9% NaCl solution); (ii) PDRN (8 mg⁄ kg); (iii) DMPX (3,7-dimethyl-1-propargilxanthine, 0.1 mg⁄ kg); or (iv) PDRN (8 mg⁄ kg) +DMPX (0.1 mg⁄ kg). Animals were euthanized at 1, 7 and 30 days following reperfusion. Vascular endothelial growth factor (VEGF) expression is normally associated with adenosine A2A receptor stimulation. After treatment, VEGFmRNA⁄ protein expression quantified by qPCR and Western blot, vascular endothelial growth factor receptor-1 (VEGFR1) and endothelial nitric oxide synthase ...
Press Release issued Jul 24, 2014: Reportstack, provider of premium market research reports announces the addition of Vascular Endothelial Growth Factor D (VEGF-D) Inhibitors -Pipeline Insights, 2014 market report to its offering DelveInsights,Vascular Endothelial Growth Factor D (VEGF-D) Inhibitors-Pipeline Insights, 2014, report provides comprehensive insights about pipeline drugs across this mechanism of action (MOA).
Ovarian hyperstimulation syndrome (OHSS) is a major complication of fertility treatment associated with multiple follicular recruitment along with elevation of estradiol level. The cause of OHSS is not well defif ined. However, the pathophysiology of OHSS is currently believed to be mediated through vascular endothelial growth factor (VEGF). OHSS is considered an iatrogenic complication. OHSS is potentially life-threatening. The incidence of OHSS is approximately 10-20% in women undergoing ovarian stimulation for IVF. However, the incidence of severe OHSS which required hospitalization is approximately 1-2%.
OBJECTIVE: To determine the role of vascular response in the castration-induced regression of benign and malignant human prostate tissue, as recent studies show that castration rapidly decreases blood flow and induces endothelial cell death, which may be important for subsequent epithelial cell death and involution of the glandular tissue of the prostate.. MATERIALS AND METHODS: The expression of vascular endothelial growth factor (VEGF) and its receptors was analysed using the quantitative reverse transcriptase-polymerase chain reaction, in benign and tumour areas of core biopsies taken before, and approximately 1 week after castration therapy. The castration-induced VEGF response was related to therapy-induced changes in tumour cell apoptotic index and subsequent response in serum prostate-specific antigen (PSA). In another set of patients, serum VEGF was quantified by enzyme-linked immunosorbent assay before, and at 3--6 months after castration therapy.. RESULTS: VEGF mRNA was down-regulated ...
To evaluate the efficacy of selective episcleral delivery of celecoxib formulated in a sustained-release episcleral exoplant on a model of retinal and choroidal neovascularization induced in rabbits by subretinal injection of matrigel combined with vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). Nine New Zealand white rabbits were randomly assigned to three groups (episcleral celecoxib exoplant, intravitreal bevacizumab injection and control group). The bFGF was mixed with matrigel at a concentration of 10 ug/0.1 mL, and VEGF was mixed with matrigel at a concentration of 2 ug/0.1 mL. Animals assigned to celecoxib or intravitreal bevacizumab groups were treated within 03 days from matrigel injection. Fluorescein angiography (FA) and electroretinography (ERG) were performed 5 days, 2, 4 and 8 weeks after matrigel injection. Persistence or regression of three clinical features (subretinal hyperfluorescence, retinal vascular tortuosity and retinal fibrotic spots) was
en] Placental growth factor (PlGF) is an angiogenic factor that belongs to the vascular endothelial growth factor (VEGF) family. Besides its well known capacity to potentiate the angiogenic action of VEGF, PlGF also participates in inflammatory processes by attracting and activating monocytes; it plays therefore more specifically a role in pathological conditions. PIGF and its two receptors, VEGFR-1 and neuropilins (NRPs), are expressed in the brain and increase after experimental stroke, but their precise functions in the nervous system remain underexplored. In this review article, we summarize present knowledge on the role of PlGF in various nervous system disease processes. Given the available data, P1GF has neuroprotective and neurotrophic properties that make it an actor of considerable interest in the pathophysiology and potentially in the therapy of degenerative and traumatic brain or spinal cord diseases ...
Two new studies published in the Journal of Clinical Oncology suggest that women who had high levels of vascular endothelial growth factor (VEGF), a protein produced by breast cancer cells, may be more likely to suffer recurrences or die from the disease than are women with low levels of VEGF. Cancerous tumors depend on surrounding blood vessels for nourishment for growth, and VEGF stimulates the growth of blood vessels. In the first study, conducted at Swedens Umed University Hospital, researchers studied 525 women with breast cancer that was invasive, but had not spread to the womans lymph nodes. After following the women for an average of just under four years, researchers found that women with high VEGF levels were almost 3 times more likely to die than those with lower VEGF levels. The second study of 305 women conducted by doctors at the University Womens Clinic in Basel, Switzerland, found that women with higher VEGF levels were more likely to suffer a relapse or recurrence of breast ...
In 2015, the standard treatment for most patients with advanced kidney cancer was a vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) such as sunitinib or pazopanib for untreated patients, followed by a checkpoint inhibitor (PD-1 inhibitor) such as nivolumab for patients who fail treatment with a VEGF inhibitor. However, over the last several years, there has been a raft of clinical trials showing that if you combine VEGF inhibitors with PD-1 inhibitors, you can get better outcomes than with a VEGF inhibitor alone.. This paper discusses how the standard of care for untreated patients with advanced renal cell carcinoma (RCC) has shifted from a VEGF TKI alone to a combination of checkpoint inhibitor plus either a VEGF TKI or a CTLA-4 inhibitor.. Read more in Oncology Nursing News here. ...
Both advanced glycation end products and vascular endothelial growth factor are believed to play a role in the pathogenesis of diabetic retino pathy. It is known that vascular endothelial growth facto
Medical therapy has failed to make any significant impact on survival in pancreatic cancer. Non Steroidal Anti-inflammatory Drugs (NSAIDs) have shown promise in several gastrointestinal (Gl) cancers. Evidence has suggested a similar effect in pancreatic cancer. Cyclooxygenase-2 (COX-2), a major target of NSAIDs, is upregulated in pancreatic cancer and is associated with worse prognosis. COX-2 upregulation has been shown to correlate with angiogenesis and production of pro- angiogenic growth factors, especially Vascular Endothelial Growth Factor (VEGF), in several Gl cancers. Although this relationship between COX-2 and angiogenesis in pancreatic cancer would seem a viable target, clinical trials of COX-2 or VEGF inhibitors have demonstrated no survival benefit ...
PRIMARY OBJECTIVE:. I. To determine the effect of two different doses of AVE0005 (vascular endothelial growth factor [VEGF] Trap [ziv-aflibercept]) treatment on the progression-free proportion at 8 weeks in patients with metastatic renal cell carcinoma who had previous treatment with a tyrosine kinase inhibitor (TKI).. SECONDARY OBJECTIVES:. I. To determine the effect of AVE0005 (VEGF Trap) treatment on objective response rate in patients with metastatic renal cell carcinoma who have had previous TKI treatment.. II. To describe progression-free survival among patients who undergo dose escalation following progression on low-dose AVE0005 (VEGF Trap).. III. To evaluate the safety and tolerability of AVE0005 (VEGF Trap) in patients with metastatic renal cell carcinoma who have had previous treatment with a TKI.. OTHER PRE-SPECIFIED OBJECTIVES:. I. To determine the circulating levels of VEGF AVE0005 (VEGF-Trap) complex and correlate it with clinical activity.. II. To evaluate the modulation of ...
TY - JOUR. T1 - Paclitaxel (Taxol). T2 - An inhibitor of angiogenesis in a highly vascularized transgenic breast cancer. AU - Lau, Derick H. AU - Xue, Ling. AU - Young, Lawrence J.. AU - Burke, Patricia A.. AU - Cheung, Anthony T.. PY - 1999. Y1 - 1999. N2 - Paclitaxel (Taxol), a promoter of microtubule polymerization and a radiosensitizing agent, is one of the more active anticancer drugs in the current treatment of solid tumors. In this study, we show that paclitaxel possesses an antiangiogenic property associated with a down-regulation of vascular endothelial growth factor (VEGF) in a highly-vascularized transgenic murine breast cancer (Met-1). Paclitaxel, at non-cytotoxic doses of 0, 3 and 6 mg/kg/day, was administered intraperitoneally for 5 days to nude mice bearing the Met-1 breast tumor. Extent of intratumoral angiogenesis, as indicated by microvessel tortuosity and microvessel density, was significantly reduced by paclitaxel in a dose-dependent manner. Paclitaxel also suppressed ...
Psoriasin (S100A7), a member of the S100 family of calcium-binding proteins, is highly expressed in high-grade ductal carcinoma in situ (DCIS) and in the benign hyper-proliferative skin disorder psoriasis. Both breast cancer and psoriasis are diseases which are characterized by hyperproliferation and a disturbed differentiation of the epithelial cells as well as a pronounced angiogenesis. The potential role of psoriasin in angiogenesis and the epithelial differentiation remain unclear.. The aim of this thesis was to investigate the cellular effects of psoriasin in angiogenesis and the differentiation processes, with special emphasis on breast cancer and psoriasis.. We found that psoriasin expression was induced in mammary epithelial cells and keratinocytes by oxidative stress. Psoriasin expression was shown to induce vascular endothelial growth factor (VEGF) expression and several other pro-angiogenic factors in epithelial cells. Upon down-regulation of psoriasin, H2O2-induced expression of VEGF ...
TY - JOUR. T1 - Differences between rat strains in models of retinopathy of prematurity. AU - Floyd, Beth N I. AU - Leske, David A.. AU - Wren, Siobhan M E. AU - Mookadam, Martina. AU - Fautsch, Michael P. AU - Holmes, Jonathan M. PY - 2005/7/19. Y1 - 2005/7/19. N2 - Purpose: Genetic factors appear to modulate the incidence and severity of retinopathy of prematurity (ROP). Different rat strains may be analogous to genetic differences across human ethnic groups. We investigated the incidence and severity of neovascularization (NV) in Brown Norway (BN) and Sprague Dawley (SD) rats in oxygen-induced retinopathy (OIR) and acidosis-induced retinopathy (AIR) models for ROP. We also studied whether there was a difference in retinal vascular endothelial growth factor (VEGF) mRNA levels in OIR animals. Methods: Newborn SD and BN rats (110 in both groups) were raised in standardized litters of ten (four OIR, twelve AIR, six non-gavaged room air controls). Beginning on day 1 of life, OIR litters were ...
Breakdown of the blood-brain barrier (BBB) or inner blood-retinal barrier (BRB), induced by pathologically elevated levels of vascular endothelial growth factor (VEGF) or other mediators, can lead to vasogenic edema and significant clinical problems such as neuronal morbidity and mortality, or vision loss. Restoration of the barrier function with corticosteroids in the brain, or by blocking VEGF in the eye are currently the predominant treatment options for brain edema and diabetic macular edema, respectively. However, corticosteroids have side effects, and VEGF has important neuroprotective, vascular protective and wound healing functions, implying that long-term anti-VEGF therapy may also induce adverse effects. We postulate that targeting downstream effector proteins of VEGF and other mediators that are directly involved in the regulation of BBB and BRB integrity provide more attractive and safer treatment options for vasogenic cerebral edema and diabetic macular edema. The endothelial cell-specific
Microdialysate fluid from 145 severely injured NSICU-patients, 88 with subarachnoidal haemorrage (SAH), and 57 with traumatic brain injury (TBI), was collected by microdialysis during the first 7 days following impact, and levels of the neurotrophins fibroblast growth factor-2 (FGF2) and vascular endothelial growth factor (VEGF) were analysed. The study illustrates both similarities and differences in the reaction patterns of the 2 inflammatory proteins. The highest concentrations of both FGF2 and VEGF were measured on Day 2 (mean (+/- SE) values being 47.1 +/- 15.33 and 116.9 +/- 41.85 pg/ml, respectively, in the pooled patient material). The VEGF concentration was significantly higher in TBI-patients, while the FGF2 showed a tendency to be higher in SAH-patients. This is the first report presenting in some detail the human cerebral response of FGF2 and VEGF following SAH and TBI. Apart from increasing the understanding of the post-impact inflammatory response of the human brain, the study ...
Spotlight on bevacizumab and its potential in the treatment of malignant pleural mesothelioma: the evidence to date Pavel A Levin,1 Jonathan E Dowell1,2 1Division of Hematology/Oncology, University of Texas Southwestern Medical Center, 2Section of Hematology/Oncology, Veteran Affairs North Texas Health Care System, Dallas, TX, USA Abstract: Malignant pleural mesothelioma (MPM) is a rare, but aggressive cancer. Surgery and radiation offer limited benefit, and systemic chemotherapy remains the primary treatment modality for the majority of patients. Vascular endothelial growth factor (VEGF) and its receptor have been recognized as important players in the biology of this disease. Bevacizumab is a monoclonal antibody that binds VEGF and blocks its interaction with the VEGF receptor. Recent studies have shown benefit with the addition of bevacizumab to the combination of cisplatin and pemetrexed in MPM. This combination is now included in the National Comprehensive Cancer Network guidelines (with a
TY - JOUR. T1 - Decrease in circulating endothelial progenitor cells in treated glioma patients. AU - Corsini, Elena. AU - Ciusani, Emilio. AU - Gaviani, Paola. AU - Silvani, Antonio. AU - Canazza, Alessandra. AU - Bernardi, Gaetano. AU - Calatozzolo, Chiara. AU - Meco, Francesco Di. AU - Salmaggi, Andrea. PY - 2012/5. Y1 - 2012/5. N2 - High-grade gliomas are highly vascularized tumors, in which the amount of new blood vessels is closely related with the degree of malignancy. The role of endothelial progenitor cells (EPCs) in the neoangiogenesis of gliomas and the effects of post-surgical therapies (i.e., radiotherapy (RT) and chemotherapy) have not yet been fully elucidated. The aim of the present study was to evaluate the effect of surgery and post-surgical treatment on the levels of circulating EPCs in glioma patients and their correlation with vascular endothelial growth factor (VEGF). In this study, we assessed by flow cytometry the number of EPCs in the peripheral blood of 78 high-grade ...
Vasculogenesis, Angiogenesis and Endothelial Cell Differentiation. The embryonic vasculature forms by the segregation, migration and assembly of angioblasts from mesoderm, a process termed vasculogenesis. Angiogenesis continues vascular development by forming new vessels by sprouting from preexisting vessels. Two growth factors that play important roles in angioblast differentiation and vessel assembly are basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF). Our hypothesis is that FGF induces angioblast differentiation and both FGF and VEGF play major roles in the further growth and morphogenesis of angioblasts into the initial vascular pattern. Angioblasts in quail embryos and in quail/chick chimeras can be visualized using the monoclonal antibody, QH-1. The classic embryological technique of microsurgical transplantation will be used in combination with modern immunohistochemistry and molecular biology to perturb vasculogenesis and angiogenesis. Small beads and ...
Notch receptors are important mediators of cell fate during embryogenesis, but their role in adult physiology, particularly in postnatal angiogenesis, remains unknown. Of the Notch receptors, only Notch1 and Notch4 are expressed in vascular endothelial cells. Here we show that blood flow recovery and postnatal neovascularization in response to hindlimb ischemia in haploinsufficient global or endothelial-specific Notch1(+/-) mice, but not Notch4(-/-) mice, were impaired compared with wild-type mice. The expression of vascular endothelial growth factor (VEGF) in response to ischemia was comparable between wild-type and Notch mutant mice, suggesting that Notch1 is downstream of VEGF signaling. Treatment of endothelial cells with VEGF increases presenilin proteolytic processing, gamma-secretase activity, Notch1 cleavage, and Hes-1 (hairy enhancer of split homolog-1) expression, all of which were blocked by treating endothelial cells with inhibitors of phosphatidylinositol 3-kinase/protein
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Vascular endothelial growth factor (VEGF) is a key player in the pathogenesis of neovascular age-related macular degeneration (nAMD) and is also involved in the final common pathway of antidepressant medication. This study investigated the relationship between the need for anti-VEGF retreatment in patients with nAMD and antidepressant medication, and the potential impact of ocular structural factors. Data from two identical prospective 2-year treatment protocols using ranibizumab or aflibercept in a variable-dosing regimen (Observe-and-Plan) were analysed. Retreatment requirement was compared with antidepressant medication intake (primary outcome) and a variety of ocular factors from baseline and from month 3 response (secondary outcomes), using univariate and multivariate analyses. Of the 206 included patients (227 eyes), 19 were on antidepressant medication. Their nAMD eyes significantly more often had pigment epithelium detachment (PED, p=0.04). Multivariate analysis revealed a si
TY - JOUR. T1 - Mitochondrial UQCRB regulates VEGFR2 signaling in endothelial cells. AU - Jung, Hye Jin. AU - Kim, Yonghyo. AU - Chang, Junghwa. AU - Kang, Sang Won. AU - Kim, Jeong Hun. AU - Kwon, Ho Jeong. N1 - Funding Information: Acknowledgments We are grateful to Young-Guen Kwon for technical assistance with the Matrigel plug assay and Paul Schumacker, Natalie Ahn, and James Chen for critical comments. This study was partly supported by grants from the National Research Foundation of Korea funded by the Korean Government (MEST; 2009-0092964, 2010-0017984, 2012M3A9D1054520), the Translational Research Center for Protein Function Control, KRF (2009-0083522), the Center for Food and Drug Materials of Agriculture Science & Technology Development (PJ0079772012), Rural Development Administration, National R&D Program, Ministry of Health &Welfare (0620360-1), and the Brain Korea 21 Project, Republic of Korea.. PY - 2013/9. Y1 - 2013/9. N2 - Vascular endothelial growth factor (VEGF) signal ...
Aggressive pituitary tumors (APTs) are associated with significant morbidity and mortality, and effective treatment options are limited. Immune checkpoint inhibitors (ICIs) have revolutionized clinical cancer care; however, there is little experience with these agents in the management of APTs. Vascular endothelial growth factor (VEGF) targeted therapy has reported success in a small number of APT case reports. Here we describe a case of pituitary carcinoma responding to ICI therapy and subsequently VEGF inhibition. We discuss the possible mechanisms and experience with ICI therapy and VEGF inhibitors in the management of APTs, biomarkers that may predict response, and the potential role of combination therapies including ICIs and temozolomide.
Anti-vascular endothelial growth factor (VEGF)[edit]. *Bevacizumabα. Medicines for reproductive health and perinatal care[edit] ... 21.6 Anti-vascular endothelial growth factor (VEGF). *22 Medicines for reproductive health and perinatal care *22.1 ...
Another agent involved in autocrine cancer signaling is vascular endothelial growth factor (VEGF). VEGF, produced by carcinoma ... Weigand, Melanie; Hantel, Pia; Kreienberg, Rolf; Waltenberger, Johannes (2005). "Autocrine vascular endothelial growth factor ... One approach used by tumors to upregulate growth and survival is through autocrine production of growth and survival factors. ... For example, despite widespread expression of epidermal growth factor receptors (EGFRs) and EGF family ligands in non-small- ...
... vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and transforming growth factor-β (TGF-β). These ... Feb 2007). "Vascular endothelial growth factor-targeted therapy in renal cell carcinoma: current status and future directions ... "Vascular Endothelial Growth Factor", Madame Curie Bioscience Database, Landes Bioscience, retrieved January 25, 2012. ... "Cannabinoids Inhibit the Vascular Endothelial Growth Factor Pathway in Gliomas". Cancer Research. 64 (16): 5617-5623. doi: ...
An association with vascular endothelial growth factor has been observed.[4] Prognosis[edit]. Prognosis and treatment is the ...
Vascular endothelial growth factor (VEGF) seems to play a vital role in promoting neovascularization. Using anti-VEGF drugs ( ... "Anti-vascular endothelial growth factor (VEGF) drugs for treatment of retinopathy of prematurity". The Cochrane Database of ... "Injections of anti-vascular endothelial growth factor for advanced diabetic retinopathy , Cochrane". The Cochrane Database of ... antibodies to sequester the growth factor), research have shown significant reduction in the extent of vessel outgrowth. Low ...
"Homologs of vascular endothelial growth factor are encoded by the poxvirus orf virus". Journal of Virology. Retrieved 9 ... of this is the pox virus vaccinia which encoded a viral growth factor similar that is very similar to the human growth factor ... "Parasite-intrinsic factors can explain ordered progression of trypanosome antigenic variation". Proc Natl Acad Sci U S A. 104 ... suggests that the ordered appearance of different VSG variants is controlled by at least two key parasite-derived factors: ...
... epidermal growth factor; EGFR, epidermal growth factor receptor; MoAbs, monoclonal antibodies; VEGF, vascular endothelial ... factor for BPA in skin of 2.5. A relative biological effectiveness (RBE) or CBE factor of 3.2 has been used in all tissues for ... growth factor. The major challenge in the development of boron delivery agents has been the requirement for selective tumor ... Biological weighting factors have been used in all of the recent clinical trials in patients with high grade gliomas, using ...
"Anti-vascular endothelial growth factor for macular oedema secondary to central retinal vein occlusion". Cochrane Database Syst ...
Vascular endothelial growth factor 1. Isner JM. Therapeutic angiogenesis: a new frontier for vascular therapy. Vasc Med. 1996 1 ... Spatiotemporal control over growth factor signaling for therapeutic neovascularization. Adv Drug Deliv Rev. 2007 Nov 10;59(13): ...
... epidermal growth factor receptor; MoAbs, monoclonal antibodies; VEGF, vascular endothelial growth factor. The major challenge ... Ono, Koji (28 March 2016). "An analysis of the structure of the compound biological effectiveness factor". Journal of Radiation ... In vivo growth suppression of experimental melanoma solid tumor". Cancer Letters. 150 (2): 177-82. doi:10.1016/S0304-3835(99) ...
... anti-vascular endothelial growth factors and photodynamic therapy. Ophthalmologists are using anti-vascular endothelial growth ... Nielsen J. S.; Fick T. A.; Saggau D. D.; Barnes C. H. (2012). "Intravitreal anti-vascular endothelial growth factor therapy for ... factors to treat AMD and similar conditions since research indicates that vascular endothelial growth factor (VEGF) is one of ... the causes for the growth of the abnormal vessels that cause these conditions.[citation needed] ...
Yi ZY, Feng LJ, Xiang Z, Yao H (2011). "Vascular endothelial growth factor receptor-1 activation mediates epithelial to ... conditional inactivation of the β-catenin gene in endothelial cells causes a defective vascular pattern and increased vascular ... to specifically have vascular endothelium cells deficient in β-catenin showed disrupted adhesion between vascular endothelial ... homeostasis and growth, also make it susceptible to alterations that can lead to abnormal cell behavior and growth. Any changes ...
"Constitutive production and thrombin-induced release of vascular endothelial growth factor by human megakaryocytes and ... When platelets are recruited to a site in the blood vessel they can release a variety of growth factors (PDGF,[51] VEGF,[52] ... Assoian, R. K.; Komoriya, A.; Meyers, C. A.; Miller, D. M.; Sporn, M. B. (1983-06-10). "Transforming growth factor-beta in ... "Role of Ras Signaling in the Induction of Snail by Transforming Growth Factor-β". Journal of Biological Chemistry. 284 (1): 245 ...
"Entrez Gene: FLT1 fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)". ... Vascular endothelial growth factor receptor 1 is a protein that in humans is encoded by the FLT1 gene. Oncogene FLT belongs to ... Shibuya M (2007). "Vascular endothelial growth factor receptor-1 (VEGFR-1/Flt-1): a dual regulator for angiogenesis". ... FLT1 has been shown to interact with PLCG1 and vascular endothelial growth factor B (VEGF-B). VEGF receptors GRCh38: Ensembl ...
Lee J, Gray A, Yuan J, Luoh SM, Avraham H, Wood WI (March 1996). "Vascular endothelial growth factor-related protein: a ligand ... This gene encodes a tyrosine kinase receptor for vascular endothelial growth factors C and D. The protein is thought to be ... Petrova TV, Makinen T, Alitalo K (November 1999). "Signaling via vascular endothelial growth factor receptors". Experimental ... "Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and VEGF receptor 3 ( ...
"Vascular endothelial growth factor gene therapy - HSCI". Adis Insight. Springer Nature Switzerland AG. "Gene Therapy for PAD ... it delivers the gene encoding for vascular endothelial growth factor (VEGF). Neovasculogen is a plasmid encoding the CMV ...
"Neuropilin-1 is expressed by endothelial and tumor cells as an isoform-specific receptor for vascular endothelial growth factor ... Gluzman-Poltorak Z, Cohen T, Shibuya M, Neufeld G (June 2001). "Vascular endothelial growth factor receptor-1 and neuropilin-2 ... January 2002). "Selective upregulation of vascular endothelial growth factor receptors neuropilin-1 and -2 in human ... "Vascular endothelial growth factor (VEGF) and its receptors". FASEB Journal. 13 (1): 9-22. doi:10.1096/fasebj.13.1.9. PMID ...
... such as Von Willebrand factor and vascular endothelial growth factor (VEGF). These substances could also have a role in PDP ... 2000). "Vascular endothelial growth factor and hypertrophic osteoarthropathy". Clin Exp Rheumatol. 18 (1): 57-62. PMID 10728444 ... platelet-derived growth factor (PDGF) and epidermal growth factor (EGF). It has not been described yet what role these ... Von Willebrand factor is a marker of platelet and endothelial activation. This suggests that the activation of endothelial ...
Genetic amplification of the vascular endothelial growth factor (VEGF) pathway genes, including VEGFA, in human osteosarcoma. „ ... Transforming growth factor-beta as a key molecule triggering the expression of versican isoforms v0 and v1, hyaluronan synthase ... Expression of transforming growth factor beta isoforms in osteosarcoma variants: association of TGF beta 1 with high-grade ... Regulatory controls for osteoblast growth and differentiation: role of Runx/Cbfa/AML factors. „Crit Rev Eukaryot Gene Expr". 14 ...
cell growth. • cell-substrate adhesion. • vascular endothelial growth factor receptor signaling pathway. • cell adhesion. • ... vascular endothelial growth factor receptor 2 binding. • fibronectin binding. • virus receptor activity. • extracellular matrix ... positive regulation of vascular endothelial growth factor receptor signaling pathway. • positive regulation of protein ... fibroblast growth factor binding. • insulin-like growth factor I binding. • C-X3-C chemokine binding. • integrin binding. • ...
Some growth factors, such as vascular endothelial growth factor, are also capable of directly acting as mitogens, causing ... Other well-known mitogenic growth factors include platelet derived growth factor (PDGF) and epidermal growth factor (EGF). ... This is not true for all growth factors, as some growth factors instead appear to cause mitogenic effects like growth ... "Vascular Endothelial Growth Factor is a Secreted Angiogenic Mitogen". 8 December 1989, Science, Vol. 246, pp 1306-1309. Morgan ...
Mousa SA, Mousa SS (June 2010). "Current status of vascular endothelial growth factor inhibition in age-related macular ... Ferrara N, Adamis AP (June 2016). "Ten years of anti-vascular endothelial growth factor therapy". Nature Reviews. Drug ... Examples of RNA aptamer molecular targets and potential targets include vascular endothelial growth factor, osteoblasts, and C- ... For instance, siRNA can be used to target mRNAs that code for proteins that promote tumor growth such as the VEGF receptor and ...
Vascular endothelial growth factor (VEGF) and enhanced green fluorescent protein (EGFP) cDNA was ligated to either side of an ... Leung, D.; Cachianes, G; Kuang, W.; Goeddel, D.; Ferrara, N (1989). "Vascular endothelial growth factor is a secreted ... engineered cells produce a bioluminescent marker and a chemotactic growth factor. In this instance, increased fluorescence of ... A key factor that differentiates molecular processors is "the ability to control output" of protein or peptide concentration as ...
"High lactate dehydrogenase 5 expression correlates with high tumoral and stromal vascular endothelial growth factor expression ... These ROS drive cancer cell proliferation by activating kinases that drive cell cycle progression growth factors at low ... Expression of LDH5 and VEGF in tumors and the stroma has been found to be a strong prognostic factor for diffuse or mixed-type ... shifting use of glucose metabolites from simple energy production to the promotion of accelerated cell growth and replication. ...
2000). "HCPTPA, a protein tyrosine phosphatase that regulates vascular endothelial growth factor receptor-mediated signal ...
The repression of the vascular endothelial growth factor (VEGF) can also cause glomerular TMA (damage to the glomerular ... Leukocyte adhesion to the damaged endothelial wall and abnormal von Willebrand factor (or vWF) release can also contribute to ... The cytotoxicity from the lack of protein damages glomerular endothelial cells by creating voids in the endothelial wall and ... Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial ...
April 2005). "Vascular endothelial growth factor in pleural effusions of different origin". Eur. Respir. J. 25 (4): 600-4. doi: ... been shown to be raised in malignant pleural effusions compared to benign disease include vascular endothelial growth factor ( ... Clinical factors predicting the diagnosis of malignant pleural effusions are symptoms lasting more than 1 month and the absence ...
Endothelial_Growth_Factor_Receptor - the Vascular Endothelial Growth Factor Receptor Structure in Interactive 3D Biology portal ... July 2008). "Vascular endothelial growth factor-A is a survival factor for nucleus pulposus cells in the intervertebral disc". ... "Neuropilin-1 is expressed by endothelial and tumor cells as an isoform-specific receptor for vascular endothelial growth factor ... Vascular endothelial growth factor (VEGF) is an important signaling protein involved in both vasculogenesis (the formation of ...
It works by slowing the growth of new blood vessels by inhibiting vascular endothelial growth factor A (VEGF-A), in other words ... Its development was based on the discovery of human vascular endothelial growth factor (VEGF), a protein that stimulated blood ... Ferrara N (2011). "From the discovery of vascular endothelial growth factor to the introduction of avastin in clinical trials ... Ribatti D (2008). "Napoleone Ferrara and the saga of vascular endothelial growth factor". Endothelium. 15 (1): 1-8. doi:10.1080 ...
It has been hypothesized that vascular endothelial growth factor may cause the vascular permeability at the root of HACE.[16] ... These factors cause the brain to swell with fluid, resulting in severe impairment.[14] If the swelling is untreated, it causes ... This in turn can increase vascular permeability and causes edema. This may combine with low levels of cytokines to cause HACE.[ ...
2007) Transforming growth factor (TGF)-beta1 stimulates pulmonary fibrosis and inflammation via a Bax-dependent, bid-activated ... of both alveolar ventilation and cardiac output because bronchial and vascular functions are altered by injury-related factors ... The core pathology is disruption of the capillary-endothelial interface: this actually refers to two separate barriers - the ... 2007) Transforming growth factor (TGF)-beta1 stimulates pulmonary fibrosis and inflammation via a Bax-dependent, bid-activated ...
The developmental morphogenesis of the canal was sensitive to the inhibition of lymphangiogenic growth factors, and in adults, ... a unique mechanism involving the transdifferentiation of venous endothelial cells in the eye into lymphatic-like endothelial ... "Schlemm's canal is a unique vessel with a combination of blood vascular and lymphatic phenotypes that forms by a novel ... the administration of the lymphangiogenic growth factor VEGFC enlarged the Schlemm's canal, which was associated with a ...
"Neuropilin-1 binds vascular endothelial growth factor 165, placenta growth factor-2, and heparin via its b1b2 domain". J. Biol ... "Neuropilin-1 is expressed by endothelial and tumor cells as an isoform-specific receptor for vascular endothelial growth factor ... Fuh G, Garcia KC, de Vos AM (2000). "The interaction of neuropilin-1 with vascular endothelial growth factor and its receptor ... 2002). "Somatic mutation of vascular endothelial growth factor receptors in juvenile hemangioma.". Genes Chromosomes Cancer 33 ...
Anna Dorothea Wagner, Christoph Thomssen, Johannes Haerting, Susanne Unverzagt: Vascular-endothelial-growth-factor (VEGF) ... Quantifying antivascular effects of monoclonal antibodies to vascular endothelial growth factor: insights from imaging. In: ... Vascular Endothelial Growth Factor) ein.[4]. Bevacizumab ist ein Angiogenesehemmer, der zielgerichtet an den Wachstumsfaktor ... phase III trial of chemotherapy with or without bevacizumab for first-line treatment of human epidermal growth factor receptor ...
... where they induce IFN production with the presence of a particular transcription factor and activate transcription factor 2. ... endothelial cells (via passive diffusion/ osmosis & active selection). P-glycoprotein (mechanism by which active transportation ... Neutrophil granules contain a variety of toxic substances that kill or inhibit growth of bacteria and fungi. Similar to ... Some products of the coagulation system can contribute to the non-specific defenses by their ability to increase vascular ...
Mutations in TGFBI which encodes transforming growth factor beta induced cause several forms of corneal dystrophies including ... Congenital hereditary endothelial dystrophy. Treatment[edit]. Early stages may be asymptomatic and may not require any ... Congenital hereditary endothelial corneal dystrophy is characterized by a diffuse ground-glass appearance of both corneas and ... They are not caused by outside factors, such as injury or diet. ... X-linked endothelial corneal dystrophy. The following (now ...
... is a pegylated anti-vascular endothelial growth factor (VEGF) aptamer, a single strand of nucleic acid that binds ... This then reduces the growth of the blood vessels located within the eye and works to control the leakage and swelling.[2] ... pegaptanib was successful at blocking VEGF-mediated vascular leakage almost entirely. The sustained release of the drug was ... Additional growth factors: Adrenomedullin. *Colony-stimulating factors (see here instead). *Connective tissue growth factor ( ...
Endothelial dysfunction is implicated in many aspects of vascular diseases. The researchers noted that the effect of vitamin C ... Hypoxia-inducible factor-proline dioxygenase enzymes (isoforms: EGLN1, EGLN2, and EGLN3)[95][96] ... "L-ascorbic Acid: a multifunctional molecule supporting plant growth and development". Scientifica. 2013: 1-24. doi:10.1155/ ... One of these was thought to be the anti-scorbutic factor. In 1928, this was referred to as "water-soluble C," although its ...
"Vascular endothelial growth factor B, a novel growth factor for endothelial cells". Proc. Natl. Acad. Sci. U.S.A. 93 (6): 2567- ... Other growth factors in this family include vascular endothelial growth factors B and C (VEGF-B, VEGF-C)[16][17] which are ... "Vascular endothelial growth factor: A new member of the platelet-derived growth factor gene family". Biochemical and ... Platelet-derived growth factor (PDGF) is one among numerous growth factors that regulate cell growth and division. In ...
Growth factor. See here instead.. Insulin. *Agonists: Chaetochromin (4548-G05). *Insulin-like growth factor 1 ... It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also ... Moreover, endothelial cells have been described as a potential source for this B1 receptor-CXCL5 pathway.[11] ... Sérgio Henrique Ferreira, discovered a bradykinin-potentiating factor (BPF) in the bothropic venom, which increases powerfully ...
endothelial cell apoptotic process. • positive regulation of vascular smooth muscle cell proliferation. • negative regulation ... Clark IA (June-August 2007). "How TNF was recognized as a key mechanism of disease". Cytokine Growth Factor Rev. 18 (3-4): 335- ... TNF, DIF, TNF-alpha, TNFA, TNFSF2, Tumour necrosis factor, TNF-α, tumor necrosis factor, TNLG1F, Tumor necrosis factor alpha. ... Tumor necrosis factor (TNF, tumor necrosis factor alpha, TNFα, cachexin, or cachectin) is a cell signaling protein (cytokine) ...
... a brain-derived neurotrophic factor that function in nerve growth and maintenance within the brain.[86][20]. *Vorinostat (SAHA) ... on global DNA and neprilysin genes in murine cerebral endothelial cells". primary. Biochemical and Biophysical Research ... a neurotrophic factor important for long-term memory.[66] Expression of CREB, an activity-dependent transcription factor ... IL-6 and transforming growth factor-alpha levels are elevated in ventricular cerebrospinal fluid in juvenile parkinsonism and ...
A major fetal growth factor in contrast to Insulin-like growth factor 1, which is a major growth factor in adults."[5] ... A major fetal growth factor in contrast to Insulin-like growth factor 1, which is a major growth factor in adults. ... It is believed to be a major fetal growth factor in contrast to Insulin-like growth factor 1, which is a major growth factor in ... Vascular endothelial. *VEGF-A. *VEGF-B. *VEGF-C. *VEGF-D. *PGF. Other. *Nerve ...
... or the growth of new blood vessels has been reported to correspond with MM progression where vascular endothelial growth factor ... This disrupts the positive feedback loop between the two growth factors, possibly causing both multiple birth defects and anti- ... resulting in accumulation of the ligase substrates and downregulation of fibroblast growth factor 8 (FGF8) and FGF10. ... Thalidomide was discovered to inhibit tumour necrosis factor-alpha (TNF-α) in 1991. TNF-α is a cytokine produced by macrophages ...
Newer agents such as anti Vascular Endothelial Growth Factor (anti VEGF) are also associated with similar injuries, as well as ... "Hypertension Induced by Vascular Endothelial Growth Factor Signaling Pathway Inhibition: Mechanisms and Potential Use as a ... But there is a body of evidence that several factors including apoptosis-induction seem to play a role.[17] ... In order to be a match for a kidney transplant, patients must match blood type and human leukocyte antigen factors with their ...
Hattori R, Hamilton KK, Fugate RD, McEver RP, Sims PJ (May 1989). "Stimulated secretion of endothelial von Willebrand factor is ... is also synthesized by vascular endothelial cells and is localized in Weibel-Palade bodies". J. Clin. Invest. 84 (1): 92-9. doi ... platelet and helps cancer cells invade into bloodstream for metastasis and provided locally with multiple growth factors ... "Differential regulation of endothelial exocytosis of P-selectin and von Willebrand factor by protease-activated receptors and ...
Abrupt increase in systemic vascular resistance, likely related to humoral vasoconstrictors. *Endothelial injury and ... and thrombotic/mitotic growth factors, completing a vicious cycle of inflammatory changes.[9] If the process is not stopped, ... "Vascular Biology Working Group". Retrieved 2010-04-20.. [dead link] *^ Elliot WJ, Varon J, Bakris GL. "Drugs used for the ... Many factors and causes are contributory in hypertensive crises. The most common cause in patients with diagnosed, chronic ...
Platelet-derived growth factor. *Transforming growth factor beta superfamily. *Vascular endothelial growth factor ... Additional growth factors: Adrenomedullin. *Colony-stimulating factors (see here instead). *Connective tissue growth factor ( ... Growth factors. *Epidermal growth factor. *Fibroblast growth factor. *Nerve growth factor. * ... Hepatoma-derived growth factor (HDGF). *Interleukins/T-cell growth factors (see here instead) ...
... vascular endothelial growth factor (VEGF), TNF, prostaglandins, leukotrienes, and varieties of chemokines and cytokines some of ... Granule contents of basophils are abundant with histamine, heparin, chondroitin sulfate, peroxidase, platelet-activating factor ...
"Growth control of lung cancer by interruption of 5-lipoxygenase-mediated growth factor signaling". The Journal of Clinical ... Fibroblasts, smooth muscle cells and endothelial cells express low levels of ALOX5.[6][7] Up-regulation of ALOX5 may occur ... micro-vascular permeability, and mucus secretion; they likewise contribute to various allergic and non-allergic reactions ... potent chemotactic factor, LTB4, and possibly also weaker chemotactic factor, 5S-HETE, which serve to attract and otherwise ...
... such as vascular endothelial growth factor (VEGF) and inhibitors of angiogenesis, such as pigment epithelium-derived factor ( ... AAV encoding neurotrophic factors such as fibroblast growth factor (FGF) family members and GDNF either protected ... Neurotrophic factors have the ability to modulate neuronal growth during development to maintain existing cells and to allow ... Since the regulation of vascularization in the mature retina involves a balance between endogenous positive growth factors, ...
... granulocyte-macrophage-stimulating growth factor,[31] platelet-derived growth factor,[31] vascular endothelial growth factor,[ ... transforming growth factors alpha,[26] beta 1 and beta 2,[27][28] fibroblast growth factors,[29] epidermal growth factor,[30] ... "Unbound vascular endothelial growth factor and its receptors in breast, human milk, and newborn intestine". Am. J. Clin. Nutr. ... Colostrum also contains a number of growth factors, such as insulin-like growth factors I (IGF-1),[24] and II,[25] ...
... may receive bevacizumab which is a monoclonal antibody medication targeted against the vascular endothelial growth factor (VEGF ... "Non-Small Cell Lung Cancer Risk Factors". www.cancer.org.. *^ a b Liu X, Conner H, Kobayashi T, Kim H, Wen F, Abe S, Fang Q, ... mutations within epidermal growth factor (EGFR) and Anaplastic Lymphoma Kinase.[43] There are also a number of additional ... Smoking is by far the leading risk factor for lung cancer.[16] Cigarette smoke contains more than 6,000 components, many of ...
... leading some to suggest that increased levels of IL-6 and vascular endothelial growth factor (VEGF) may contribute to the ... Once the cortex (the outer shell) of the bone has been disrupted, vascular channels may invade adjacent soft tissues and joints ... Gorham and Stout found that vascular anomalies always occupied space that normally would be filled with new bone and speculated ... These complications or their symptoms, such as difficulty breathing, chest pain, poor growth or weight loss, and infection have ...
These factors lead to accumulations of genetic mutations in oncogenes (genes that control the growth rate of cells) and tumor ... There are many intravenous methods of drug delivery, known as vascular access devices. These include the winged infusion device ... such as blood vessel endothelial cells. They bind to the tumor antigen and are internalised, where the linker releases the drug ... G1 - the initial growth phase. S - the phase in which DNA is synthesised. G2 - the second growth phase in preparation for cell ...
8] RGC axons that do cross at the optic chiasm are guided by the vascular endothelial growth factor, VEGF-A, expressed at the ... Gordon-Weeks, PR (2005). Neuronal Growth Cones. Cambridge University Press. ISBN 9780511529719. .. ... This navigation is mediated by the neuronal growth cone, a structure that responds to the cues by ligand-receptor signalling ...
... and interleukin 6 may activate procoagulation factors in the cells lining blood vessels, leading to endothelial damage. The ... At least one should be drawn through the skin and one through each vascular access device (such as an IV catheter) that has ... refers to physical interventions to control a focus of infection and reduce conditions favorable to microorganism growth or ... Microbial factors[edit]. Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune ...
The biology of vascular endothelial growth factor.. Ferrara N1, Davis-Smyth T. ... Vascular Endothelial Growth Factor A. *Vascular Endothelial Growth Factors. Substances. *Endothelial Growth Factors ... Receptors, Growth Factor. *Vascular Endothelial Growth Factor A. *Vascular Endothelial Growth Factors ... Endothelial Growth Factors*/chemistry. *Endothelial Growth Factors*/genetics. *Endothelial Growth Factors*/therapeutic use ...
Vascular endothelial growth factor enhances atherosclerotic plaque progression.. Celletti FL1, Waugh JM, Amabile PG, Brendolan ... Vascular endothelial growth factor (VEGF) can promote angiogenesis but may also exert certain effects to alter the rate of ... Plaque macrophage and endothelial cell content also increased disproportionately over controls. In order to confirm that the ... Vascular Endothelial Growth Factor A. *Vascular Endothelial Growth Factors. Substances. *Apolipoprotein B-100 ...
... detected a stimulating activity of endothelial cells in the... ... Vascular Endothelial Growth Factor: The Cornerstone of Vascular ... Bikfalvi A. (2017) Vascular Endothelial Growth Factor: The Cornerstone of Vascular Development Factors. In: A Brief History of ... Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo. Nature 362(6423):841- ... Leung DW, Cachianes G, Kuang WJ, Goeddel DV, Ferrara N (1989) Vascular endothelial growth factor is a secreted angiogenic ...
... is a prime regulator of endothelial cell proliferation, angiogenesis, vasculogenesis and vascular permeability. Its activity is ... Vascular endothelial growth factor and its receptors Cytokine Growth Factor Rev. 1996 Oct;7(3):259-70. doi: 10.1016/s1359-6101( ... Vascular endothelial growth factor (VEGF) is a prime regulator of endothelial cell proliferation, angiogenesis, vasculogenesis ... Receptors, Vascular Endothelial Growth Factor * Vascular Endothelial Growth Factor A * Vascular Endothelial Growth Factors ...
Expression of two angiogenic factors, vascular endothelial growth factor and platelet-derived endothelial cell growth factor in ... Vascular permeability factor/vascular endothelial growth factor induces lymphangiogenesis as well as angiogenesis. J Exp Med. ... Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is a homodimeric 34 to 45 ... The vascular endothelial growth factor family and its receptors. Hematol Oncol Clin North Am. 2004 Oct; 18(5):951-971,vii. ...
Vascular endothelial growth factor (VEGF), an established angiogenesis factor, is expressed in allografts undergoing rejection ... In vitro, we found that VEGF enhanced endothelial cell expression of the chemokines monocyte chemoattractant protein 1 and IL-8 ... Anti-VEGF failed to inhibit T cell activation responses in vivo, but inhibited intragraft expression of several endothelial ... and in combination with IFN-γ synergistically induced endothelial cell production of the potent T cell chemoattractant IFN- ...
Vascular Endothelial Growth Factor A Inhibitor, Vascular Endothelial Growth Factor C Inhibitor, Vascular Endothelial Growth ... Vascular Endothelial Growth Factor A Inhibitor, Vascular Endothelial Growth Factor C Inhibitor, Vascular Endothelial Growth ... Vascular Endothelial Growth Factor A Inhibitor, Vascular Endothelial Growth Factor C Inhibitor, Vascular Endothelial Growth ... Vascular Endothelial Growth Factor A Inhibitor, Vascular Endothelial Growth Factor Regulator. Additional Keywords : Cannabinoid ...
Increased intraocular and systemic levels of the angiogenic factor vascular endothelial growth factor (VEGF) is associated with ... Vascular Endothelial Growth Factor (VEGF) in Uveitis. The safety and scientific validity of this study is the responsibility of ... This study will look for the presence in blood of a substance called vascular endothelial growth factor (VEGF) in patients with ... A Pilot Study to Demonstrate the Presence of Vascular Endothelial Growth Factor (VEGF) in Uveitic Cystoid Macular Edema. ...
... is a cytokine that greatly increases vascular permeability and thereby promotes hypovolemia. The present study examines whether ... Vascular endothelial growth factor (VEGF) is a cytokine that greatly increases vascular permeability and thereby promotes ... Endotoxin boosts the vascular endothelial growth factor (VEGF) in rabbits J Endotoxin Res. 2003;9(2):97-100. doi: 10.1179/ ...
VEGF-A (VEGF) is a potent growth factor for blood vessel endothelial cells, showing pleiotropic responses that facilitate cell ... is a family of closely related growth factors having a conserved pattern of eight cysteine residues and sharing common VEGF ... Role of vascular endothelial growth factor and vascular endothelial growth factor receptors in vascular development. Curr. Top ... Vascular endothelial growth factor (VEGF) is a family of closely related growth factors having a conserved pattern of eight ...
We reported that PAX6 suppresses glioblastoma cell growth in vivo and anchorage-independent growth without significant ... vascular endothelial growth factor, and epidermal growth factor receptor in gliomas: relationship to tumor grade and survival. ... Vascular endothelial growth factor A (VEGFA) is the major angiogenic factor that is overexpressed in GBM [5]. An antiangiogenic ... Because we found that PAX6 downregulates expression of the gene encoding vascular endothelial growth factor A (VEGFA) in glioma ...
Vascular endothelial growth factor and hepatocyte growth factor levels are differentially elevated in patients with advanced ... Vascular Endothelial Growth Factor in Stage V ROP. The safety and scientific validity of this study is the responsibility of ... Regulation of vascular endothelial growth factor by oxygen in a model of retinopathy of prematurity. Arch Ophthalmol. 1996 Oct; ... Vascular Endothelial Growth Factor (VEGF) is a dimeric glycoprotein, naturally expressed in epithelial and tumor cells (1). ...
... et al Vascular endothelial cell growth factor-driven endothelial tube formation is mediated by vascular endothelial cell growth ... Brown LF, Yeo KT, Berse B, Morgentaler A, Dvorak HF, Rosen S Vascular permeability factor (vascular endothelial growth factor) ... Kuroda M, Oka T, Oka Y, et al Colocalization of vascular endothelial growth factor (vascular permeability factor) and insulin ... Brown LF, Berse B, Jackman RW, et al Increased expression of vascular permeability factor (vascular endothelial growth factor) ...
"Combined analysis of vascular endothelial growth factor and platelet-derived endothelial cell growth factor expression in ... "Prognostic significance of serum levels of vascular endothelial growth factor and insulin-like growth factor-1 in advanced ... D. J. Park, N. J. Thomas, C. Yoon, and S. S. Yoon, "Vascular endothelial growth factor A inhibition in gastric cancer," Gastric ... Predictive Significance of Serum Level of Vascular Endothelial Growth Factor in Gastric Cancer Patients. Lu Wang, Yanli Chang, ...
These neuroprotective effects were related to increased vascular endothelial growth factor and CD31 expression, which promoted ... Neuroprotective Effects of Hypoxic Preconditioning Linked With Increased Vascular Endothelial Growth Factor. ...
Comparative analysis of vascular endothelial growth factor receptors on retinal and aortic vascular endothelial cells. Diabetes ... Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis. Nature. 1992; 359: 843-845. ... Vascular endothelial growth factor-121 (VEGF121) is a non-heparin-binding isoform of VEGF secreted in response to hypoxic or ... Vascular endothelial growth factor-121 (VEGF121) is an angiogenic protein secreted in response to hypoxia that binds to VEGF ...
chicken chorioallantoic membrane-derived endothelial cells;. VEGF,. vascular endothelial growth factor;. PTEN,. phosphatase and ... The levels of mRNA for vascular endothelial growth factor (VEGF) are elevated in cells expressing activated PI 3-kinase or Myr- ... Phosphatidylinositol 3-kinase signaling mediates angiogenesis and expression of vascular endothelial growth factor in ... Phosphatidylinositol 3-kinase signaling mediates angiogenesis and expression of vascular endothelial growth factor in ...
PAVES: Pegfilgrastim Anti-vascular Endothelial Growth Factor (VEGF) Evaluation Study. The safety and scientific validity of ...
... lymphangiogenesis and endothelial cell growth, stimulating their proliferation and migration and also has effects on the ... May function in the formation of the venous and lymphatic vascular systems during embryogenesis, and also in the maintenance of ... a growth factor belonging to platelet-derived growth factor/vascular endothelial growth factor family.". Avantaggiato V., ... "Identification of a c-fos-induced gene that is related to the platelet-derived growth factor/vascular endothelial growth factor ...
... vasculogenesis and endothelial cell growth. Induces endothelial cell proliferation, promotes cell migration, inhibits apoptosis ... vascular endothelial growth factor receptor 1 binding Source: GO_Central. *vascular endothelial growth factor receptor 2 ... vascular endothelial growth factor receptor 1 binding Source: GO_Central. *vascular endothelial growth factor receptor 2 ... Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth. Induces endothelial cell proliferation, ...
... cellular response to leukemia inhibitory factor (ortholog); PARTICIPATES IN vascular endothelial growth factor signaling ... vascular endothelial growth factor receptor 3 binding (ortholog); INVOLVED IN angiogenesis (ortholog); animal organ ... vascular endothelial growth factor C). NCBI. Ortholog. Mus musculus (house mouse):. Vegfc (vascular endothelial growth factor C ... vascular endothelial growth factor C) HGNC Alliance Mus musculus (house mouse) : Vegfc (vascular endothelial growth factor C) ...
Proteopedia Vascular_Endothelial_Growth_Factor - the Vascular Endothelial Growth Factor Structure in Interactive 3D. ... Vascular endothelial growth factor (VEGF), originally known as vascular permeability factor (VPF), is a signal protein produced ... Ribatti D (2005). "The crucial role of vascular permeability factor/vascular endothelial growth factor in angiogenesis: a ... "Transcriptional regulation of vascular endothelial growth factor in cancer". Cytokine Growth Factor Rev. 16 (1): 77-89. doi: ...
3 The abbreviations used are: VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor; C, ... Green Tea Catechins Inhibit Vascular Endothelial Growth Factor Receptor Phosphorylation. Sylvie Lamy, Denis Gingras and Richard ... Green Tea Catechins Inhibit Vascular Endothelial Growth Factor Receptor Phosphorylation. Sylvie Lamy, Denis Gingras and Richard ... Green Tea Catechins Inhibit Vascular Endothelial Growth Factor Receptor Phosphorylation. Sylvie Lamy, Denis Gingras and Richard ...
These immature vessels are selectively obliterated as a consequence of vascular endothelial growth factor (VEGF) withdrawal. In ... Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal ... Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal ... VEGF loss led, in turn, to selective apoptosis of endothelial cells in vessels devoid of periendothelial cells. These results ...
... ; VEGF. http://www.lymphedemapeople/thesite/vascular_endothelial_growth_factor_VEGF.htm. VEGF ... Overproduction of vascular endothelial growth factor/vascular permeability factor is causative in Crow-Fukase (POEMS) syndrome ... Assignment of vascular endothelial growth factor (VEGF) and placenta growth factor (PIGF) genes to human chromosome 6p12-p21 ... Free insulin growth factor-1 and vascular endothelial growth factor in the vitreous fluid of patients with proliferative ...
... the main regulator for the cell membrane tight junction is vascular endothelial growth factor (VEGF). This is produced by the ... Retrieved from "http://drmyhill.co.uk/drmyhill/index.php?title=Vascular_endothelial_growth_factor_(VEGF)-_salivary_test_for_ ...
Vascular endothelial growth factor, platelet-derived endothelial cell growth factor and angiogenesis in non-small-cell lung ... Brown LF, Berse B, Jackman RW, et al: Expression of vascular permeability factor (vascular endothelial growth factor) and its ... Guidi AJ, Abu-Jawdeh G, Berse B, et al: Vascular permeability factor (vascular endothelial growth factor) expression and ... Plate KH, Breier G, Weich HA and Risau W: Vascular endothelial growth factor is a potential tumour angiogenesis factor in human ...
Vascular endothelial growth factor receptor 2 (VEGFR2) is highly expressed by lymphatic endothelial cells and has been shown to ... Vascular endothelial growth factor receptor-2 promotes the development of the lymphatic vasculature.. [Michael T Dellinger, ... However, the role VEGFR2 serves in the development of the lymphatic vascular system has not been defined. Here we use the Cre- ... of the lymphatic network and further defines the molecular mechanisms controlling the development of the lymphatic vascular ...
Vascular endothelial growth factor C (VEGF-C) is a protein that is a member of the platelet-derived growth factor / vascular ... January 1998). "Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and ... January 2004). "Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic ... January 2003). "Vascular endothelial growth factor-C expression in human gallbladder cancer and its relationship to lymph node ...
  • Vascular endothelial growth factor (VEGF) can promote angiogenesis but may also exert certain effects to alter the rate of atherosclerotic plaque development. (nih.gov)
  • Vascular endothelial growth factor (VEGF) is a prime regulator of endothelial cell proliferation, angiogenesis, vasculogenesis and vascular permeability. (nih.gov)
  • Among the topics discussed are VEGF and VEGF receptor structure and bioactivity, the regulation of VEGF expression, the role of VEGF and its receptors in vascular development, and the involvement of VEGF and its receptors in normal and pathological (ocular and tumor) angiogenesis. (nih.gov)
  • Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is a homodimeric 34 to 45 kilodalton, heparin-binding glycoprotein. (labcorp.com)
  • VEGF has potent angiogenic, mitogenic, and vascular permeability-enhancing activities specific for endothelial cells. (labcorp.com)
  • 1 Tumor expression of proangiogenic factors, including VEGF, has been associated with advanced tumor progression in a number of human cancers. (labcorp.com)
  • 23 It has been hypothesized that VEGF released from activated platelets may have a role in angiogenesis during wound healing and may also be associated with pathological conditions, such as atherosclerosis, tumor growth, and metastasis formation. (labcorp.com)
  • Vascular endothelial growth factor (VEGF) is a family of closely related growth factors having a conserved pattern of eight cysteine residues and sharing common VEGF receptors. (sigmaaldrich.com)
  • VEGF-A (VEGF) is a potent growth factor for blood vessel endothelial cells, showing pleiotropic responses that facilitate cell migration, proliferation, tube formation, and survival. (sigmaaldrich.com)
  • It is also one of the most potent permeability factors, so that VEGF-A is a common link of inflammation, permeability and angiogenesis. (sigmaaldrich.com)
  • Local hypoxia is a potent inducer of VEGF-A expression from adjacent cells but it is not synthesized in endothelial cells, indicating a paracrine regulation of vessel formation. (sigmaaldrich.com)
  • VEGF-B exerts its actions through one receptor (VEGFR-1).VEGF-C, also called VEGF-related factor (VRP) or VEGF-2, in the adult is expressed primarily in the heart, placenta, lung, kidney, muscle, ovary and small intestine. (sigmaaldrich.com)
  • VEGF-D, also called c-fos induced growth factor (FIGF), is a VEGF homologue induced by c-fos. (sigmaaldrich.com)
  • Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and VEGF receptor 3 (Flt4). (sigmaaldrich.com)
  • Vascular endothelial growth factor (VEGF) and its receptors. (sigmaaldrich.com)
  • Vascular endothelial growth factor (VEGF), an established angiogenesis factor, is expressed in allografts undergoing rejection, but its function in the rejection process has not been defined. (jci.org)
  • In vitro, we found that VEGF enhanced endothelial cell expression of the chemokines monocyte chemoattractant protein 1 and IL-8, and in combination with IFN-γ synergistically induced endothelial cell production of the potent T cell chemoattractant IFN-inducible protein-10 (IP-10). (jci.org)
  • Anti-VEGF failed to inhibit T cell activation responses in vivo, but inhibited intragraft expression of several endothelial cell adhesion molecules and chemokines, including IP-10. (jci.org)
  • The vascular endothelial growth factor (VEGF) family of growth factors controls pathological angiogenesis and increased vascular permeability in important eye diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). (nih.gov)
  • When we focus on the VEGF receptors, recent findings suggest a role of VEGFR-1 as a functional receptor for placenta growth factor (PlGF) and vascular endothelial growth factor-A (VEGF)-A in pericytes and vascular smooth muscle cells in vivo rather than in endothelial cells, and strongly suggest involvement of pericytes in early phases of angiogenesis. (nih.gov)
  • This study will look for the presence in blood of a substance called vascular endothelial growth factor (VEGF) in patients with uveitis (eye inflammation). (clinicaltrials.gov)
  • Increased intraocular and systemic levels of the angiogenic factor vascular endothelial growth factor (VEGF) is associated with new vessel growth in the eye, such as diabetic retinopathy. (clinicaltrials.gov)
  • Vascular Endothelial Growth Factor (VEGF) is a dimeric glycoprotein, naturally expressed in epithelial and tumor cells (1). (clinicaltrials.gov)
  • Growth of new blood vessels (angiogenesis), required for all tumor growth, is stimulated by the expression of vascular endothelial growth factor (VEGF). (aacrjournals.org)
  • Finally, we show that VEGF 165 b expressing tumors grow significantly more slowly than VEGF 165 -expressing tumors, indicating that a switch in splicing from VEGF 165 to VEGF 165 b can inhibit tumor growth. (aacrjournals.org)
  • Angiogenesis is stimulated by the expression of vascular growth factors, the most commonly expressed of which is vascular endothelial growth factor (VEGF). (aacrjournals.org)
  • Of all of the growth factors involved in angiogenesis, VEGF appears to play an irreplaceable role. (aacrjournals.org)
  • VEGF was originally described as a growth and survival factor for endothelial cells. (aacrjournals.org)
  • Vascular endothelial growth factor (VEGF), originally known as vascular permeability factor (VPF), is a signal protein produced by fibroblasts that stimulates the formation of blood vessels. (wikipedia.org)
  • To be specific, VEGF is a sub-family of growth factors, the platelet-derived growth factor family of cystine-knot growth factors. (wikipedia.org)
  • Overexpression of VEGF can cause vascular disease in the retina of the eye and other parts of the body. (wikipedia.org)
  • In 1989 Ferrara and Henzel described an identical factor in bovine pituitary follicular cells which they purified, cloned and named VEGF. (wikipedia.org)
  • Activity of VEGF-A, as its name implies, has been studied mostly on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g., stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells). (wikipedia.org)
  • In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. (wikipedia.org)
  • VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor. (wikipedia.org)
  • Role of vascular endothelial growth factor (VEGF) and VEGF-R genotyping in guiding the metastatic process in pT4a resected gastric cancer patients," PLoS ONE , vol. 7, no. 7, Article ID e38192, 2012. (hindawi.com)
  • Vascular endothelial growth factor-121 (VEGF 121 ) is an angiogenic protein secreted in response to hypoxia that binds to VEGF receptors overexpressed by ischemic microvasculature. (ahajournals.org)
  • Vascular endothelial growth factor-121 (VEGF 121 ) is a non-heparin-binding isoform of VEGF secreted in response to hypoxic or ischemic conditions. (ahajournals.org)
  • Vascular endothelial growth factor C (VEGF-C) is a protein that is a member of the platelet-derived growth factor / vascular endothelial growth factor (PDGF/VEGF) family. (wikipedia.org)
  • The main function of VEGF-C is to promote the growth of lymphatic vessels (lymphangiogenesis). (wikipedia.org)
  • Apart from vascular targets, VEGF-C is also important for neural development and blood pressure regulation. (wikipedia.org)
  • In invertebrates, molecules from this families are not easily distinguished from each other and are collectively referred to as PVFs (PDGF/VEGF-like growth factors. (wikipedia.org)
  • The levels of mRNA for vascular endothelial growth factor (VEGF) are elevated in cells expressing activated PI 3-kinase or Myr-Akt. (pnas.org)
  • The present study demonstrates that Cr(VI) induces hypoxia-inducible factor 1 (HIF-1) activity through the specific expression of HIF-1alpha but not HIF-1beta subunit and increases the level of vascular endothelial growth factor (VEGF) expression in DU145 human prostate carcinoma cells. (cdc.gov)
  • Vascular Endothelial Growth Factor B (VEGF Related Factor or VEGFB) - Vascular endothelial growth factor B also known as VEGF-B is a protein encoded by the VEGF-B gene. (researchandmarkets.com)
  • Vascular Endothelial Growth Factor B (VEGF Related Factor or VEGFB) pipeline Target constitutes close to 15 molecules. (researchandmarkets.com)
  • The latest report Vascular Endothelial Growth Factor B - Pipeline Review, H1 2020, outlays comprehensive information on the Vascular Endothelial Growth Factor B (VEGF Related Factor or VEGFB) targeted therapeutics, complete with analysis by indications, stage of development, mechanism of action (MoA), route of administration (RoA) and molecule type. (researchandmarkets.com)
  • It also reviews key players involved in Vascular Endothelial Growth Factor B (VEGF Related Factor or VEGFB) targeted therapeutics development with respective active and dormant or discontinued projects. (researchandmarkets.com)
  • Objective To investigate the relation of circulating concentrations of vascular endothelial growth factor (VEGF) for the risk of developing cardiovascular disease (CVD) in a large community-based sample. (bmj.com)
  • Multivariable Cox proportional hazards models were estimated adjusting for standard risk factors to VEGF quartiles to incident CVD. (bmj.com)
  • Vascular endothelial growth factor (VEGF) receptors (VEGFR) play a major role in tumor angiogenesis and, thus, represent attractive targets for the development of novel anticancer therapeutics. (aacrjournals.org)
  • VEGF 3 is an endothelial cell-specific mitogen that is often associated with tumor-induced angiogenesis. (aacrjournals.org)
  • These immature vessels are selectively obliterated as a consequence of vascular endothelial growth factor (VEGF) withdrawal. (jci.org)
  • VEGF loss led, in turn, to selective apoptosis of endothelial cells in vessels devoid of periendothelial cells. (jci.org)
  • demonstrated that VEGF, also called vascular permeability factor (VPF), is produced by cultured vascular smooth muscle cells. (lymphedemapeople.com)
  • Ferrara and Henzel (1989) determined that purified bovine Vegf was mitogenic to adrenal cortex-derived capillary endothelial cells and to several other vascular endothelial cells, but it was not mitogenic toward nonendothelial cells. (lymphedemapeople.com)
  • demonstrated that culture media conditioned by human embryonic kidney cells expressing either bovine or human VEGF cDNA promoted proliferation of capillary endothelial cells. (lymphedemapeople.com)
  • VEGF, a homodimeric glycoprotein of relative molecular mass 45,000, is the only mitogen that specifically acts on endothelial cells. (lymphedemapeople.com)
  • Folkman (1995) noted the importance of VEGF and its receptor system in tumor growth and suggested that intervention in this system may provide promising approaches to cancer therapy. (lymphedemapeople.com)
  • VEGF and placental growth factor ( 601121 ) constitute a family of regulatory peptides capable of controlling blood vessel formation and permeability by interacting with 2 endothelial tyrosine kinase receptors, FLT1 ( 165070 ) and KDR/FLK1. (lymphedemapeople.com)
  • Because this is extremely hard work and the body does not want to waste energy, the main regulator for the cell membrane tight junction is vascular endothelial growth factor (VEGF). (drmyhill.co.uk)
  • Vascular endothelial growth factor (VEGF) plays an important role in many disease states, including ischemia, chronic and acute inflammation, and pathologies associated with angiogenesis such as tumors and wounds. (spandidos-publications.com)
  • A number of factors regulate VEGF promoter activity and VEGF expression such as four and a half LIM domains 1 (FHL1) and Smad4. (spandidos-publications.com)
  • The role of vascular endothelial growth factor (VEGF) in the regulation of angiogenesis has been under investigation for over a decade ( 1 ). (spandidos-publications.com)
  • The VEGF family includes VEGF-A, VEGF-B, VEGF-C, VEGF-D and placental growth factor (PlGF) in mammals ( 2 , 3 ), as well as two exogenous VEGF subtypes, VEGF-E (virus genome-encoded VEGF) and VEGF-F (snake venom-derived VEGF) ( 4 , 5 ). (spandidos-publications.com)
  • These VEGF molecules act through binding to several high-affinity transmembrane endothelial cell receptors, including Flt-1 (VEGFR1), KDR (VEGFR2) and Flt-4 (VEGFR3) with varying specificities. (spandidos-publications.com)
  • Binding of VEGF to these receptors leads to intracellular receptor phosphorylation which initiates various intracellular downstream receptor pathways, leading to endothelial cell proliferation and blood vessel formation. (spandidos-publications.com)
  • Vascular endothelial growth factor (VEGF)/vascular permeability factor is the prototype for a growing family of dimeric growth factors, which exert their effects on vascular and lymphatic endothelial cells, as well as on a wide range of other cell types. (portlandpress.com)
  • Growing tumours produce VEGF, and many different strategies for inhibiting tumour growth by inhibiting VEGF production are being tested in clinical trials at present. (portlandpress.com)
  • It is similar in structure to VASCULAR ENDOTHELIAL GROWTH FACTOR D in that they both contain N- and C-terminal extensions that were not found in other VEGF family members. (curehunter.com)
  • Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, induces endothelial proliferation in vitro and vascular permeability in vivo. (pnas.org)
  • VEGF and its receptors Flk-1/KDR and Flt-1 may play a role in vascular development and regulation of vascular permeability. (pnas.org)
  • Vascular endothelial growth factor (VEGF) is well known to play an important regulatory role in vascular growth and development. (jneurosci.org)
  • We applied VEGF to normoxic fetal organotypic cortical explants as a model of CNS neuropil, in addition to primary cortical neurons, to assess direct growth effects absent vascular or astroglial activity. (jneurosci.org)
  • Antisense oligodeoxynucleotides to flk-1 , but not flt-1 , inhibited neuritic outgrowth, whereas inhibitors of the signaling pathways MEK1 and P13-AKT both abrogated VEGF-induced growth. (jneurosci.org)
  • Possibly, VEGF achieves its effects by acting on the neuronal microtubular content, which is involved with growth, stability and maturation. (jneurosci.org)
  • Vascular endothelial growth factor (VEGF) is a secreted vascular mitogen that is purportedly specific for endothelial cells and plays an important regulatory role in vascular growth in several organ systems during development ( Ferrara and Davis-Smyth, 1997 ). (jneurosci.org)
  • Little information exists concerning the direct growth effects of the application of VEGF to CNS tissue because most work regarding VEGF action, receptor mechanisms, and signaling pathways has been done in non-neural tissues. (jneurosci.org)
  • Thus, precise growth and developmental roles for VEGF in CNS tissue are difficult to determine, particularly because the protein is markedly downregulated after birth. (jneurosci.org)
  • In the present study we have examined the neurotrophic actions of VEGF on fetal cortical explants as well as on primary cortical neurons to further assess how VEGF may directly affect neuronal growth absent any angiogenic or astroglial activity. (jneurosci.org)
  • Here, we show that vascular endothelial growth factor (VEGF) signaling profoundly affects both vascularization and innervation of the pancreatic islet. (biologists.org)
  • Using genetic mouse models, we demonstrate that VEGF regulates islet innervation indirectly through its effects on intra-islet endothelial cells. (biologists.org)
  • Our data indicate that formation of a VEGF-directed, intra-islet vascular plexus is required for development of islet innervation, and that VEGF-induced islet hypervascularization leads to increased nerve fiber ingrowth. (biologists.org)
  • VEGF111 is a recently described vascular endothelial growth factor (VEGF) isoform that does not bind to the extracellular matrix, diffuses extensively, and is resistant to proteolysis. (biomedsearch.com)
  • Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A) is a multifunctional cytokine with important roles in pathological angiogenesis. (rupress.org)
  • Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A) * is a multifunctional cytokine that has essential roles in both processes ( 5 - 8 ). (rupress.org)
  • It mediates its several activities primarily through interaction with two receptor tyrosine kinases, VEGF receptor (VEGFR)-1 and VEGFR-2, that are selectively, though not exclusively, expressed on vascular endothelium. (rupress.org)
  • Another member of the VPF/VEGF family, placenta growth factor (PlGF), also has a role in pathological angiogenesis, interacting with VEGFR-1 but not VEGFR-2 ( 9 ). (rupress.org)
  • The central molecule that directs proliferation and migration of LECs during embryogenesis is vascular endothelial growth factor C (VEGF-C). VEGF-C is therefore an important ingredient for LEC culture and attempts to (re)generate lymphatic vessels and networks. (frontiersin.org)
  • In this review, we discuss the molecular biology of VEGF-C as it relates to the growth of LECs and lymphatic vessels. (frontiersin.org)
  • The central growth factor that mediates these tasks is vascular endothelial growth factor C (VEGF-C). While being a member of the VEGF family of growth factors, VEGF-C is in many aspects very different from the vascular endothelial growth factor prototype VEGF-A. (frontiersin.org)
  • Vascular endothelial growth factor (VEGF) induces both angiogenesis and an increase in vascular permeability, 2 processes that are considered to be important for both tumor growth and the delivery of drugs to the site of tumors. (bloodjournal.org)
  • It is further shown that tmTNF is required for VEGF-mediated endothelial hyperpermeability in vitro and in vivo. (bloodjournal.org)
  • This permissive activity of TNF appears to be selective, because anti-TNF antibodies ablated the VEGF-induced permeability but not proliferation of cultivated human endothelial cells. (bloodjournal.org)
  • Furthermore, tnf gene-deficient mice show no obvious defects in vascularization and develop normally but failed to respond to administration of VEGF with an increase in vascular permeability. (bloodjournal.org)
  • Subsequent studies indicated that the tmTNF and VEGF signaling pathways converge at the level of a secondary messenger, the "stress-activated protein kinase-2" (SAPK-2)/p38: (1) up-regulated endothelial expression of tmTNF resulted in the continuous activation of SAPK-2/p38 in vitro, and (2) an inhibitor of SAPK-2/p38 activation abolished the vascular permeability activity of VEGF in vivo. (bloodjournal.org)
  • In conclusion, the study's finding that continuous autocrine signaling by tmTNF sensitizes endothelial cells to respond to VEGF by increasing their vascular permeability provides new therapeutic concepts for manipulating vascular hyperpermeability. (bloodjournal.org)
  • Vascular endothelial growth factor (VEGF) is essential for both vasculogenesis and angiogenesis 1 but was first identified as a tumor-produced vascular permeability factor (VPF) because of its potent activity in the Miles assay of vascular permeability. (bloodjournal.org)
  • 3 4 Furthermore, VEGF-induced vascular permeability has been suggested to be involved in vasculopathies of diseases different than cancer, including rheumatoid arthritis, acquired immunodeficiency syndrome, and allergic inflammation. (bloodjournal.org)
  • 5-7 In animal experiments it has been shown that the rapid induction of VEGF-mediated vascular permeability correlates with the formation of endothelial vesiculovacuolar organelles (VVOs) and fenestrations. (bloodjournal.org)
  • We also show that neutralization of TNF ablates vascular permeability, induced by VEGF in endothelial cells, in vitro and in vivo, which suggests that the ability of VEGF to induce vascular permeability is facilitated by endogenously expressed TNF. (bloodjournal.org)
  • Vascular endothelial growth factor (VEGF) plays an important role in homeostasis and diseases of the retinal pigment epithelium (RPE), choriocapillaris, and, most notably, age-related macular degeneration (AMD). (molvis.org)
  • Vascular endothelial growth factor (VEGF) was purified from media conditioned by bovine pituitary folliculostellate cells (FC). (sciencemag.org)
  • VEGF is a heparin-binding growth factor specific for vascular endothelial cells that is able to induce angiogenesis in vivo. (sciencemag.org)
  • Human 293 cells transfected with an expression vector containing a bovine or human VEGF cDNA insert secrete an endothelial cell mitogen that behaves like native VEGF. (sciencemag.org)
  • Vascular endothelial growth factor (VEGF) concentration is associated with declining lung function in 6 and 12-month studies. (mdpi.com)
  • We intended to delineate the mechanisms of erythropoietin (EPO)-induced cardiac vascular endothelial growth factor (VEGF) production and to establish if VEGF is crucial for EPO-induced improvement of cardiac performance. (rug.nl)
  • EPO stimulated VEGF mRNA expression through the signal transducers and activators of transcription-3 (STAT-3) pathway in neonatal rat cardiomyocytes, but not in endothelial cells or fibroblasts. (rug.nl)
  • Similarly, the direct effects of EPO on endothelial sprouting were modest and VEGF independent. (rug.nl)
  • VEGF neutralization attenuated EPO-induced proliferation of myocardial endothelial cells and reduced myocardial incorporation of endothelial progenitor cells (EPCs) in rats with alkaline phosphatase-labelled bone marrow cells. (rug.nl)
  • EPO fosters VEGF expression predominantly in cardiomyocytes, which in turn stimulates myocardial endothelial proliferation and incorporation of EPCs. (rug.nl)
  • Vascular endothelial growth factor (VEGF) plays a neuroprotective role in mice harboring mutations of copper-zinc superoxide dismutase 1 (SOD1) in familial amyotrophic lateral sclerosis (ALS). (jneurosci.org)
  • We postulate that the resultant dysregulation of VEGF posttranscriptional processing critically reduces the level of this neuroprotective growth factor and accelerates the neurodegenerative process in ALS. (jneurosci.org)
  • Vascular endothelial growth factor (VEGF) is considered a key mediator of tumor angiogenesis, including neovascularization in human breast cancer. (diva-portal.org)
  • In this thesis we have investigated the effects of estradiol, progesterone, and the nonsteroidal anti-estrogen tamoxifen on vascular endothelial growth factor (VEGF) and its receptors (VEGFR-1 and VEGFR-2) in normal human breast tissue, endothelial cells, and breast cancer. (diva-portal.org)
  • Conclusions- Mobilization of endothelial progenitor cells with cytokines potentiates VEGF-2 gene therapy for myocardial ischemia and enhances bone marrow cell incorporation into ischemic myocardium. (ahajournals.org)
  • Catheter-based, intramyocardial vascular endothelial growth factor (VEGF) gene transfer has been shown to induce therapeutic angiogenesis in preclinical models of myocardial ischemia 1,2 and to increase exercise tolerance time and decrease the incidence of anginal episodes in pilot studies in patients with chronic myocardial ischemia. (ahajournals.org)
  • 9,10 Recent clinical data have revealed that VEGF gene transfer is also accompanied by the mobilization of BM-derived endothelial progenitor cells (EPCs). (ahajournals.org)
  • This test measures the amount of vascular endothelial growth factor (VEGF) in your blood. (brighamandwomens.org)
  • VEGF is a substance that helps encourage the growth of new blood vessels. (brighamandwomens.org)
  • But VEGF also plays a role in cancer growth. (brighamandwomens.org)
  • Vascular endothelial growth factor (VEGF) is a potent inducer of endothelial cell growth and angiogenesis. (ovid.com)
  • The study addressed the role for aldose reductase (AR) in 1 ) retinal oxidative stress and vascular endothelial growth factor (VEGF) overexpression in early diabetes, and 2 ) high glucose-induced oxidative stress in retinal endothelial cells. (diabetesjournals.org)
  • Furthermore, our earlier ARI study in long-term galactose-fed rats ( 2 ) and a more recent antioxidant study in short-term diabetic rats ( 17 ) revealed the capacity of both classes of agents to prevent increased expression of retinal vascular endothelial growth factor (VEGF). (diabetesjournals.org)
  • VEGF has been implicated in the increased vascular permealibity, breakdown of the blood-retinal barrier, and vascular cell proliferation characteristic of DR ( 18 ). (diabetesjournals.org)
  • To explore the in vivo anti-angiogenesis effects resulting from lentivirus-mediated RNAi of vascular endothelial growth factor (VEGF) in monkeys with iris neovascularization (INV). (molvis.org)
  • A gene on chromosome 5q35.3 that encodes a tyrosine kinase receptor for vascular endothelial growth factors (VEGF) C and D, which appear to play a role in lymphangiogenesis and maintenance of the lymphatic endothelium. (thefreedictionary.com)
  • Angiogenesis is critical to tumor growth and metastasis and is dependent on growth factors, such as vascular endothelial growth factor (VEGF). (eurekaselect.com)
  • The most characterized angiogenic factor, VEGF is an endothelial cell mitogen and permeability factor that has been found to be overexpressed in almost all human cancers. (eurekaselect.com)
  • In a number of tumor model systems, antagonism of the VEGF pathway results in inhibition of angiogenesis and tumor growth. (eurekaselect.com)
  • Specifically, VEGF inhibition has been shown to suppress tumor growth, decrease microvasculature, and induce apoptosis of endothelial cells. (eurekaselect.com)
  • This close relationship between hypoxia, angiogenesis, and tumor growth makes VEGF and VEGF receptors attractive targets for anti-neoplastic therapies. (eurekaselect.com)
  • AIMS/BACKGROUND: Vascular endothelial growth factor (VEGF) is a hypoxia induced angiogenic factor. (bmj.com)
  • Thus, VEGF may function as a linking factor between retinal ischaemia and PDR associated neovascularisation. (bmj.com)
  • The article discusses a research that suggests that choroidal neovascularization and retinal exudation in patients with choroidal osteoma can be regulated with anti-vascular endothelial growth factor (VEGF) therapy. (ebscohost.com)
  • The article discusses a research study which showed the effectiveness of anti-vascular endothelial growth factor (VEGF) therapy in the treatment of patients with myopic choroidal neovascularization (CNV). (ebscohost.com)
  • The article focuses on the study on anti-vascular endothelial growth factor (anti-VEGF) as treatment option for other retinal diseases. (ebscohost.com)
  • Accordingly, VEGF plays a role in abnormal formation of blood vessels and vascular permeability. (ebscohost.com)
  • The article features the study made by Dr. Scott Cousins on the efficacy of E10030 anti-platelet-derived growth factor (PDGF) from Ophthotech Corp. and Lucentis anti-vascular endothelial growth factor (VEGF) agent from Genentech Inc. in Fort Lauderdale, Florida. (ebscohost.com)
  • The article discusses the role of anti-vascular endothelial growth factor (VEGF) therapy in treatment of corneal neovascularization. (ebscohost.com)
  • Vascular endothelial growth factor (VEGF) is a potent stimulatory factor of angiogenesis and a negative prognostic indicator of breast cancer. (diva-portal.org)
  • The aim of the present study was to evaluate the effect of GnRH analogues on the in-vitro eutopic endometrial cell apoptosis and release of interleukin-1beta (IL-1beta) and vascular endothelial growth factor (VEGF). (unboundmedicine.com)
  • To understand the pathogenetic mechanisms of endometriosis by examining the expression of adhesion molecules (CD44s), angiogenic factor (VEGF) and matrix protease and to perform Ki-67 labeling for evaluation of proliferative activity. (unboundmedicine.com)
  • CRH increased cAMP and induced secretion of vascular endothelial growth factor (VEGF) without tryptase, histamine, IL-6, IL-8, or TNF-α release. (jimmunol.org)
  • A transnational collaborative network dedicated to the study and applications of the vascular endothelial growth factor-A in medical practice: the VEGF Consortium" Clinical Chemistry and Laboratory Medicine (CCLM) , vol. 56, no. 4, 2018, pp. 83-86. (degruyter.com)
  • Vascular endothelial growth factor (VEGF) targeted therapy has reported success in a small number of APT case reports. (frontiersin.org)
  • Vascular endothelial growth factor (VEGF) is a potent vascular permeability factor and a mediator of brain edema. (ajtmh.org)
  • We carefully examine the regulating mechanisms of vascular endothelial growth factor (VEGF) and angiopoietins (Ang1 and Ang2) on the proliferation, migration and maturation of endothelial cells through their endothelium-specific receptor tyrosine kinase VEGFR2 and Tie2, respectively. (aimsciences.org)
  • We have previously shown in vitro that vascular endothelial growth factor (VEGF), produced by almost all tumors, is one of the tumor-derived factors responsible for the defective function of these cells. (bloodjournal.org)
  • Infusion of VEGF was associated with inhibition of the activity of the transcription factor NF-κB in bone marrow progenitor cells. (bloodjournal.org)
  • Experiments in vitro showed that VEGF itself, and not factors released by VEGF-activated endothelial cells, affected polypotent stem cells resulting in the observed abnormal hematopoiesis. (bloodjournal.org)
  • 9-11 Several soluble factors have been implicated in defective DC maturation in cancer, including vascular endothelial growth factor (VEGF). (bloodjournal.org)
  • 12 13 VEGF stimulates the proliferation of endothelial cells and plays an important role in the formation of tumor neovasculature. (bloodjournal.org)
  • 8 VEGF binds to hematopoietic progenitor CD34 + cells through one of the VEGF-specific receptors (Flt-1) and inhibits the activation of transcription factor NF-κB in these cells. (bloodjournal.org)
  • We ask in this study whether recombinant VEGF alone at relevant concentrations would cause significant alterations in DC development in vivo in otherwise healthy animals, which cell populations would be most affected, and what role other factors may play in the effects mediated by VEGF. (bloodjournal.org)
  • It was recently shown that vascular endothelial growth factor (VEGF), a growth factor for endothelial cells, plays a pivotal role in rheumatoid arthritis. (jimmunol.org)
  • These results show that VEGF is a key factor in pannus development, acting through the VEGF-RI pathway. (jimmunol.org)
  • It was recently demonstrated that vascular endothelial growth factor (VEGF) plays a pivotal role in RA ( 1 , 2 , 3 ). (jimmunol.org)
  • VEGF is a growth factor for endothelial cells, it also increases vascular permeability. (jimmunol.org)
  • Immunohistochemical and in situ hybridization studies of synovial tissues have shown that VEGF is strongly expressed by subsynovial macrophages, fibroblasts surrounding microvessels, vascular smooth muscle cells, and synovial lining cells ( 7 , 8 , 9 , 10 , 11 ). (jimmunol.org)
  • Vascular endothelial growth factor (VEGF) is expressed in both tumor and stromal cells in gastric cancer. (karger.com)
  • Our aim was to study the prognostic effect of LDH5, and tumoral and stromal expression of the angiogenic factor VEGF in gastric cancer, and the intercorrelation of tissue expression of both factors. (karger.com)
  • The results of our study showed that high LDH5 and VEGF expression in both tumor and stroma was a prognostic factor for patients with gastric cancers, especially diffuse- or mixed-type cancers. (karger.com)
  • Aerobic glycolysis has been shown to be under the direct control of hypoxia-inducible factors (HIF-1α and 2α) in the transcription of a variety of genes involved in angiogenesis, glycolysis, and apoptosis, including vascular endothelial growth factor (VEGF) and LDHA [ 8 ]. (karger.com)
  • The effect of vascular endothelial growth factor (VEGF) on skin flap survival and its ability to induce a pharmacological delay by promoting angiogenesis in a flap was studied in a rat transverse rectus abdominis musculocutaneous flap, using a 3 x 8-cm skin paddle with the inferior epigastric vessels as its main vascular supply. (biomedsearch.com)
  • We have recently observed lower levels of vascular endothelial growth factor (VEGF) in ovarian cancer patients with greater social support, whereas higher VEGF was found in patients with greater distress. (aacrjournals.org)
  • VEGF is primarily produced by tumor cells, endothelial cells, and platelets (11 , 12 , 13 , 14) , and works by stimulating endothelial cells in microvessels to proliferate, migrate, and alter their pattern of gene expression. (aacrjournals.org)
  • This suggests that angiogenesis is an important mediator of the behaviour of breast tumours.A protein called vascular endothelial growth factor (VEGF) has been described which is a potent inducer of angiogenesis. (gla.ac.uk)
  • It is a specific endothelial mitogen produced by both normal tissues and tumours.Prior to commencement of this thesis the role of VEGF in breast cancer had not been reported. (gla.ac.uk)
  • Vascular endothelial growth factor (VEGF) is one such potent angiogenic factor. (spandidos-publications.com)
  • Factors involved in the control of VEGF production by glioma cells are not well known. (spandidos-publications.com)
  • In this study, we investigated the role of basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and platelet derived growth factors (PDGF) on VEGF production by four different glioma cell lines in vitro. (spandidos-publications.com)
  • With the exception of PDGF A/A and B/B in one cell line, all growth factors differentially stimulated VEGF production in all cell lines investigated. (spandidos-publications.com)
  • These data suggest that VEGF production in human glioma may be regulated by other growth factors which are also known to be expressed in such tumours. (spandidos-publications.com)
  • Vascular endothelial growth factor (VEGF) is an important mediator of angiogenesis and vascular permeability. (aacrjournals.org)
  • The purpose of the present study was to measure the levels of VEGF, IL-8, and angiogenin in malignant pleural effusions and to investigate the role of these cytokines in the induction of vascular permeability in in vivo animal studies. (aacrjournals.org)
  • VEGF, also known as vascular permeability factor, is a unique angiogenic dimeric glycoprotein with a molecular mass of 34-42 kDa. (aacrjournals.org)
  • The results suggest the implication of VEGF family and their receptors in the periapical immune response, vascular remodeling and in bone resorptive activities. (uib.no)
  • At the gene level, significant up-regulations were recorded for genes involved in VEGF-mediated angiogenic activity, such as phosphatidylinositol-3-kinases (Pl3K), protein kinase C (PKC), mitogen-activated protein kinases (MAPK) and phospholipases (PL). These findings suggest the implication of VEGF family in ongoing immune reactions along with vascular remodeling in human established periapical lesions. (uib.no)
  • The pulpal tissue has high VEGF signaling capacity with respect to immune responses and vascular activity. (uib.no)
  • We used a tetracycline-regulated transgenic system to test whether the induction of vascular endothelial growth factor (VEGF) in the germinal matrix leads to intracranial hemorrhage. (sciencemag.org)
  • Vascular endothelial growth factor D (VEGF-D) is a ligand for VEGF receptor 2 (VEGFR-2) and for VEGFR-3, which are predominantly expressed on blood vascular endothelial cells and on lymphatic endothelial cells, respectively. (helsinki.fi)
  • Thus VEGF-D can contribute to growth of both blood vessels (angiogenesis) and lymphatic vessels (lymphangiogenesis). (helsinki.fi)
  • The goal of this study was to produce and purify high quality biologically active VEGF-D which is needed for studying the physiological role of this growth factor. (helsinki.fi)
  • The (P)RR-mediated dual activation of tissue RAS and RAS-independent signalling pathways, referred to as the receptor-associated prorenin system (RAPS), was shown to facilitate vascular endothelial growth factor (VEGF)-driven pathogenesis of non-proliferative DR in mice. (bmj.com)
  • We further reported that the intravitreal levels of soluble form of (P)RR (s(P)RR), released from neovascular endothelial cells in fibrovascular tissues, increased in the patients with proliferative DR (PDR) and correlated with vitreous prorenin and VEGF levels. (bmj.com)
  • Vascular endothelial growth factor (VEGF) promotes vascular permeability (VP) and neovascularization, and is required for development. (rupress.org)
  • In cultured endothelial cells, VEGF, but not basic fibroblast growth factor, promotes the Src-mediated phosphorylation of FAK on tyrosine 861, which contributes to the formation of a FAK/αvβ5 signaling complex. (rupress.org)
  • To investigate the mechanism by which the VEGF pathway coordinates with integrin αvβ5 and Src kinase, an in vivo angiogenesis model was used with a defined growth factor input, (i.e. (rupress.org)
  • Blocking or inhibiting VEGF helps prevent further growth of the blood vessels that the cancer needs to continue growing. (natmedtalk.com)
  • The activation of adenosine receptors results in the synthesis of HIF-1 and VEGF, proteins critically important for the growth and stability of cancer cells. (natmedtalk.com)
  • VEGF, as we know, stimulates the growth of blood vessels into tissues. (natmedtalk.com)
  • Although hypoxia stimulates the synthesis and release of VEGF, adenosine stimulates the synthesis and release of BOTH VEGF and IL-8, another powerful angiogenesis factor. (natmedtalk.com)
  • To test the hypothesis that 20-HETE increases endothelial cell (EC) proliferation via vascular endothelial growth factor (VEGF), we studied the effects of WIT003 [20-hydroxyeicosa-5( Z ),14( Z )-dienoic acid], a 20-HETE analog on human macrovascular or microvascular EC. (aspetjournals.org)
  • In normal tissues, blood vessel growth is regulated through a complex balance between the actions of proangiogenic factors [e.g., vascular endothelial growth factor (VEGF)] and angiogenic inhibitors. (aspetjournals.org)
  • VEGF is a crucial factor in the regulation of angiogenesis. (aspetjournals.org)
  • VEGF is the most important angiogenic molecule associated with neovascularization and a key regulator of vascular EC sprouting ( Carmeliet, 2004 ). (aspetjournals.org)
  • VEGF expression is regulated by a number of external factors. (aspetjournals.org)
  • Vessel formation as well as the levels of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α) were decreased at the damaged site in tPA −/− mice. (physiology.org)
  • The fibrinolytic system activates the tissue proteolytic system and modulates the release of growth factors from extracellular matrix, such as vascular endothelial growth factor (VEGF) ( 22 , 31 ). (physiology.org)
  • We hypothesized that vascular endothelial growth factor (VEGF) released from a coil promotes clot organization, hyperplasia, and endothelial proliferation to facilitate closure of the aneurysm neck. (ajnr.org)
  • Vascular endothelial growth factor (VEGF) is a heparin-binding glycoprotein that also functions as a vascular permeability factor (8, 9) . (ajnr.org)
  • VEGF is produced by macrophages, endothelial cells, and smooth muscle cells (9) and is currently under intense investigation for its therapeutic effectiveness in elevating collateral flow in areas of myocardial ischemia. (ajnr.org)
  • Therefore, an angiogenesis-promoting factor such as VEGF may enhance fibrosis and subsequent aneurysm obliteration in a similar hemodynamic environment. (ajnr.org)
  • The vascular endothelial growth factor (VEGF) receptor-1 (VEGFR-1) is a tyrosine kinase receptor that does not play a relevant role in physiologic angiogenesis in adults, whereas it is important in tumor angiogenesis. (aspetjournals.org)
  • The mAb is able to inhibit chemotaxis and extracellular matrix invasion of glioma cells in vitro stimulated by VEGF-A and by the VEGFR-1-selective ligand placental growth factor (PlGF). (aspetjournals.org)
  • Vascular endothelial growth factor (VEGF) is a potent endothelial mitogen that results in angiogenesis when overexpressed in human subjects. (portlandpress.com)
  • 1-5 Authors: Sengul Samanci N, Poturoglu S, Samanci C, Ustabasioglu FE, Koldas M, Duman AE, Ormeci AC Abstract Background: We evaluated ocular hemodynamic changes, malondialdehyde(MDA) and vascular endothelial growth factor (VEGF) levels in patients with IBD.Methods: We used ocular color Doppler ultrasonography to analyze 56 eyes with Crohn's disease (CD), 62 eyes with ulcerative colitis (UC), 68 eyes of healthy volunteers. (medworm.com)
  • Vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have been strongly implicated in the growth and metastasis of gastric cancer. (aacrjournals.org)
  • The purpose of this study was to examine the effects of ZD6474, an inhibitor of inhibitor of VEGF receptor (VEGFR) tyrosine kinase with additional activity against EGF receptor (EGFR), on tumor growth and angiogenesis in an orthotopic model of gastric cancer. (aacrjournals.org)
  • In addition, VEGF-mediated activation of VEGFR2 and Erk-1/2 was decreased in human umbilical vascular endothelial cells. (aacrjournals.org)
  • The roles of vascular endothelial growth factor (VEGF) and its receptors as important mediators in endothelial cell proliferation, migration, invasion, and differentiation during angiogenesis have been well established ( 4 ). (aacrjournals.org)
  • The authors evaluated the neuroprotective and angiogenic effects of a continuous and low-dose infusion of vascular endothelial growth factor (VEGF)-165 on cerebral ischemia in rats. (thejns.org)
  • It has been shown that expression of the potent angiogenic factor, vascular endothelial growth factor (VEGF), and its receptors, flt-1 (VEGFR-1) and KDR/Flk-1 (VEGFR-2), increased during the development of liver fibrosis. (bmj.com)
  • Our in vitro study showed that VEGF treatment significantly stimulated proliferation of both activated hepatic stellate cells (HSC) and sinusoidal endothelial cells (SEC). VEGF also significantly increased α1(I)-procollagen mRNA expression in activated HSC. (bmj.com)
  • The expression of different vascular endothelial growth factor (VEGF) genes was studied in glioma U87 cells with endoplasmic reticulum-nuclei-1 (ERN1) loss of function and its regulation by hypoxia and glutamine or glucose deprivation conditions as model of ischemia. (scirp.org)
  • No antiapoptotic or angiogenic influence of pioglitazone was detected while a reduced expression of hypoxia-inducible factor-3 alpha and PPAR coactivator-1 alpha (PGC-1 alpha) mRNA as well as vascular endothelial growth factor (VEGF) protein possibly occurred as a consequence of improved vascularization. (uni-muenchen.de)
  • VEGF-D (c-fos-induced growth factor) is a member of the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family and is active in angiogenesis, lymphangiogenesis and endothelial cell growth. (neuromics.com)
  • Systemic vascular endothelial growth factor A (VEGF A) neutralization ameliorates diet induced metabolic dysfunction. (centenary.org.au)
  • The vascular endothelial growth factor (VEGF) family of cytokines are important regulators of angiogenesis that have emerged as important targets for the treatment of obesity. (centenary.org.au)
  • This phenotype was caused by epithelial activation of vascular endothelial growth factor (VEGF) via recruitment of Lef1 to the promoter of VEGF. (lu.se)
  • Elevated expression of VEGF and activation of the VEGF receptor through phosphorylation promoted an increase in the proliferation rate of epithelial and endothelial cells. (lu.se)
  • Objective: Vascular endothelial growth factor (VEGF) acts, in part, by triggering calcium ion (Ca2+) entry. (whiterose.ac.uk)
  • Approach and Results: Measurement of intracellular Ca2+ in human umbilical vein endothelial cells detected a Synta66-resistant component of VEGF-activated Ca2+ entry that occurred within 2 minutes after VEGF exposure. (whiterose.ac.uk)
  • Orai3 knockdown was inhibitory for VEGF-dependent endothelial tube formation in Matrigel in vitro and in vivo in the mouse. (whiterose.ac.uk)
  • Conclusions: VEGF signaling via arachidonic acid and arachidonic acid metabolism causes Orai3 to accumulate at the cell surface to mediate Ca2+ entry and downstream endothelial cell remodeling. (whiterose.ac.uk)
  • In this paper we show that vascular endothelial growth factor (VEGF), a potent inducer of new blood vessels and vascular permeability in vivo, stimulated the migration of endothelial cells after artificial monolayer wounding and induced an increase in paracellular permeability of human umbilical vein endothelial cells (HUVECs). (biologists.org)
  • 15 minutes to 1 hour after VEGF stimulation the endothelial adherens junction components VE-cadherin, beta-catenin, plakoglobin, and p120 were maximally phosphorylated on tyrosine, while alpha-catenin was not modified. (biologists.org)
  • In contrast, activation of VEGF-receptor-1 (Flt-1) by its specific ligand placenta growth factor (PlGF) had no effect on the tyrosine phosphorylation of cadherins and catenins. (biologists.org)
  • Kim KJ, Li B, Winer J, Armanini M, Gillett N, Phillips HS, Ferrara N (1993) Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo. (springer.com)
  • Vascular permeability factor/vascular endothelial growth factor induces lymphangiogenesis as well as angiogenesis. (labcorp.com)
  • The purpose of this review is to develop new insights into the cell biology of VEGFs and vascular cells in angiogenesis and vascular leakage in general, and to provide the rationale and possible pitfalls of inhibition of VEGFs as a therapy for ocular disease. (nih.gov)
  • Because we found that PAX6 downregulates expression of the gene encoding vascular endothelial growth factor A (VEGFA) in glioma cells, we used a subcutaneous xenograft model to verify PAX6 suppression of VEGFA-induced angiogenesis based on CD31-immunostaining of endothelial cells. (springer.com)
  • Since glioma cells with stable expression of ectopic PAX6 cDNA showed dramatically suppressed growth in vivo, but no significant alteration of cell proliferation in vitro, it appears that PAX6 suppression of glioma tumorigenicity is mediated through changes in the tumor microenvironment, e.g. suppression of tumor angiogenesis. (springer.com)
  • They are important signaling proteins involved in both vasculogenesis (the de novo formation of the embryonic circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature). (wikipedia.org)
  • described a factor secreted by tumors causing angiogenisis and called it tumor angiogenesis factor. (wikipedia.org)
  • These neuroprotective effects were related to increased vascular endothelial growth factor and CD31 expression, which promoted angiogenesis. (medindia.net)
  • Growth factor active in angiogenesis, lymphangiogenesis and endothelial cell growth, stimulating their proliferation and migration and also has effects on the permeability of blood vessels. (uniprot.org)
  • Growth factor active in angiogenesis, vasculogenesis and endothelial cell growth. (uniprot.org)
  • Angiogenesis (blood vessel growth), lymphangiogenesis (lymph system growth) are all intrinsically connected with lymphedema and share many of the same genes. (lymphedemapeople.com)
  • Angiogenesis, the formation of new blood vessels sprouting from the pre-existing vasculature, is pivotal for the growth of solid tumors and also plays a critical role in invasion and metastasis. (spandidos-publications.com)
  • Gene targeting shows that most, if not all, of the factors and receptors in this family serve critical functions during vascular development or in adult physiological and pathological angiogenesis. (portlandpress.com)
  • Nitric Oxide Stimulates Vascular Endothelial Growth Factor Production in Cardiomyocytes Involved in Angiogenesis. (thefreedictionary.com)
  • Nitric oxide enhances angiogenesis via the synthesis of vascular endothelial growth factor and cGMP after stroke in the rat. (thefreedictionary.com)
  • Isoform 111 of Vascular Endothelial Growth Factor (VEGF111) Improves Angiogenesis of Ovarian Tissue Xenotransplantation. (biomedsearch.com)
  • Sex steroid exposure constitutes a risk factor for breast cancer, but little is known about the effects of sex steroids on factors mediating angiogenesis, the development of new blood vessels, in normal and malignant breast tissue. (diva-portal.org)
  • 12-16 Together, these data suggest that administration of exogenous angiogenic growth factors may stimulate both angiogenesis and vasculogenesis for therapeutic neovascularization. (ahajournals.org)
  • Danielle Hsu, Jason M. Shohet and Eugene S. Kim, "Targeting Vascular Endothelial Growth Factor in Neuroblastoma", Current Angiogenesis (Discontinued) (2013) 2: 30. (eurekaselect.com)
  • L. Arakelyan, V. Vainstein and Z. Agur, A computer algorithm describing the process of vessel formation and maturation, and its use for predicting the effects of anti-angiogenic and anti-maturation therapy on vascular tumor growth ,, Angiogenesis , 5 (2002), 203. (aimsciences.org)
  • Clearly, adenosine is fundamentally important in promoting angiogenesis and, subsequently, cancer cell growth and development. (natmedtalk.com)
  • In this study, we have investigated the influence of D16F7 on glioma growth and angiogenesis in vivo using C6 glioma cells transfected with the human VEGFR-1. (aspetjournals.org)
  • In conclusion, therapies such as ZD6474 that target two distinct aspects of tumor growth, angiogenesis and tumor cell proliferation, warrant further investigation. (aacrjournals.org)
  • One target for new therapies is angiogenesis, the dynamic process by which the blood supply of a tumor is created from preexisting blood vessels and endothelial precursor cells ( 3 , 4 ). (aacrjournals.org)
  • 7, 8 Emerging evidence has shown that angiogenesis plays a pivotal role in many physiological and pathological processes, such as tumour growth, arthritis, psoriasis, and diabetic retinopathy. (bmj.com)
  • We hypothesize that a microsphere/hydrogel combination system could be useful for the local and sustained delivery of recombinant human vascular endothelial growth factor (rhVEGF) to enhance angiogenesis in vivo . (springer.com)
  • Pattersonand C, Runge MS. Therapeutic myocardial angiogenesis via vascular endothelial growth factor gene therapy: Moving on down the road. (springer.com)
  • Nicosia R, Nicosia S, Smith M. Vascular endothelial growth factor, platelet-derived growth factor, and insulin-like growth factor-1 promote rat aortic angiogenesis in vitro . (springer.com)
  • Overexpression of VEGFA as well as PFKFB4, PFKFB3 and hexokinase 2 is an obligatory factor of tumor cell glycolysis and increased angiogenesis and proliferation [8-14]. (scirp.org)
  • Interendothelial junctions play an important role in the regulation of endothelial functions, such as vasculogenesis, angiogenesis, and vascular permeability. (biologists.org)
  • Our results demonstrate that the endothelial adherens junction is a downstream target of VEGFR-2 signaling and suggest that tyrosine phosphorylation of its components may be involved in the the loosening of cell-cell contacts in established vessels to modulate transendothelial permeability and to allow sprouting and cell migration during angiogenesis. (biologists.org)
  • 1977 ). Migration and proliferation of endothelial cells in preformed and newly formed blood vessels during tumor angiogenesis. (biologists.org)
  • 1992 ). Expression of vascular endothelial growth factor during embryonic angiogenesis and endothelial cell differentiation. (biologists.org)
  • By double immunostaining of Ki-67 and von Willebrand factor, we demonstrated that proliferating endothelial cells were found in 83% of the VEGF111 group compared with 33% in the control group (P=0.001). (biomedsearch.com)
  • Plouet J, Schilling J, Gospodarowicz D (1989) Isolation and characterization of a newly identified endothelial cell mitogen produced by AtT-20 cells. (springer.com)
  • Leung DW, Cachianes G, Kuang WJ, Goeddel DV, Ferrara N (1989) Vascular endothelial growth factor is a secreted angiogenic mitogen. (springer.com)
  • In contrast, vascular endothelial growth factor is a mitogen primarily for vascular endothelial cells. (lymphedemapeople.com)
  • We reported that PAX6 suppresses glioblastoma cell growth in vivo and anchorage-independent growth without significant alteration of cell proliferation in vitro, suggesting that PAX6 may alter the tumor microenvironment. (springer.com)
  • This study demonstrates that tmTNF is present in the endothelium of methylcholanthrene (meth A) sarcomas and that the expression of tmTNF in endothelial cells in vitro is linked to an autocrine continuous activation of these cells. (bloodjournal.org)
  • In vitro studies were performed on bovine retinal endothelial cells (BREC) cultured in either 5 or 30 mmol/l glucose with or without 1 μmol/l fidarestat. (diabetesjournals.org)
  • We investigated the role of GDF6 in promoting endothelial vascular integrity in vivo in zebrafish and in cultured human umbilical vein endothelial cells in vitro. (diva-portal.org)
  • To test this hypothesis, we examined the effects of exogenous 20-HETE or a noncyclooxygenase-metabolizable analog, WIT003 [20-hydroxyeicosa-5( Z ),14( Z )-dienoic acid], on human umbilical vein endothelial cells (HUVEC) and dermal microvascular endothelial cells (HDMVEC) in vitro. (aspetjournals.org)
  • In vitro , ZD6474 inhibited human umbilical vascular endothelial cell and TMK-1 human gastric tumor cell proliferation in a dose-dependent fashion. (aacrjournals.org)
  • Endothelial cell proliferation was significantly enhanced when cells were cultured with the rhVEGF-releasing combination system in vitro . (springer.com)
  • In some microvascular tissues, the result is pathologic neovascularization and increased vascular permeability. (diabetesjournals.org)
  • Both AR inhibitors (ARIs) and antioxidants prevent formation of retinal pericyte ghosts and acellular capillaries ( 1 , 6 , 10 ), increased vascular permeability ( 11 , 12 , 13 ), decreased blood flow and oxygenation ( 7 , 14 ), and impaired leukocyte-endothelial cell interactions resulting in retinal inflammation ( 15 , 16 ). (diabetesjournals.org)
  • However, the coordination of inputs from growth factor receptors leading to the selective recruitment or activation of specific integrins in vivo remains poorly understood. (rupress.org)
  • The ex vivo levels of nitric oxide production, inducible nitric oxide synthase, vascular endothelial cell growth factor-C and caspase-3 were also estimated to investigate the possible mechanisms of hepatoprotection. (ijpsonline.com)
  • Neovascularization is essential for tumour growth and is mediated by physiological substances produced by tumours. (spandidos-publications.com)
  • Induces endothelial cell proliferation, promotes cell migration, inhibits apoptosis and induces permeabilization of blood vessels. (uniprot.org)
  • Risau W (1996) What, if anything, is an angiogenic factor? (springer.com)
  • In addition to being an angiogenic factor it can act on LYMPHATIC VESSELS to stimulate LYMPHANGIOGENESIS. (curehunter.com)
  • Aggressive pituitary tumors (APTs) including pituitary carcinomas (PCs) are a subset of pituitary tumors with a more aggressive course defined clinically by significant invasion, rapid tumor growth rate, and resistance to optimal standard therapies ( 1 ). (frontiersin.org)
  • Their involvement in pathologic processes such as tumor growth or inflammatory disorders has been thoroughly described, rheumatoid arthritis being just one example. (uib.no)
  • Endoplasmic reticulum stress as well as hypoxia is an important factor of tumor growth. (scirp.org)
  • We also demonstrate by in situ hybridization that Flk-1 protein expression in the mouse embryo is restricted to the vascular endothelium and the umbilical cord stroma. (pnas.org)
  • bone morphogenetic protein 13) in vascular integrity although GDF6's mechanism of action was not clear. (diva-portal.org)
  • Besides, the thioacetamide-injected groups treated with methanol extract of A. shikokiana and isoepoxypteryxin exhibited a significant increase in the level of caspase-3 protein and a significant decrease of inducible nitric oxide synthase and vascular endothelial cell growth factor C levels when compared with hepatocellular carcinoma group. (ijpsonline.com)
  • This protein is structurally and functionally similar to vascular endothelial growth factor C. (neuromics.com)
  • 1991 ). Interaction of vasculotropin/vascular endothelial cell growth factor with human umbilical vein endothelial cells: binding, internalization, degradation, and biological effects. (biologists.org)
  • Waltenberger J, Claesson-Welsh L, Siegbahn A, Shibuya M, Heldin CH (1994) Different signal transduction properties of KDR and Flt1, two receptors for vascular endothelial growth factor. (springer.com)
  • May function in the formation of the venous and lymphatic vascular systems during embryogenesis, and also in the maintenance of differentiated lymphatic endothelium in adults. (uniprot.org)
  • This study demonstrates that transmembrane expression of tumor necrosis factor (tmTNF) is up-regulated in the endothelium of a murine methylcholanthrene (meth A)-induced sarcoma in comparison to the adjacent normal dermal vasculature and is also present on cultivated human endothelial cells. (bloodjournal.org)
  • Diseases of the Aorta Lab, Center for the Endothelium, Vascular Biology Program, Centenary Institute and University of Sydney, Sydney, Australia (R.L. (ahajournals.org)
  • GDF6-deficient endothelium has increased vascular endothelial growth factor signaling, increased vascular endothelial-cadherin Y658 phosphorylation, vascular endothelial-cadherin delocalization from cell-cell interfaces, and weakened endothelial cell adherence junctions that become prone to vascular leak. (diva-portal.org)
  • This FAK/αvβ5 complex was also detected in epidermal growth factor-stimulated epithelial cells, suggesting a function for this complex outside the endothelium. (rupress.org)
  • 1 In general, the growth and spread of tumors has been shown to be dependent on the development of increased vascularization in the tumor vicinity in order to maintain sufficient oxygenation. (labcorp.com)
  • identified a vascular permeability factor secreted by tumors in guinea pigs and hamsters. (wikipedia.org)
  • 8 An increase of vascular permeability has 2 important consequences for potential therapeutic interventions in tumors: First, it facilitates drug delivery 9 and, secondly, it contributes to the formation of hemorrhagic necroses, which are induced by the administration of the soluble form of tumor necrosis factor-α (TNF), both in experimental tumor models and in isolated limb perfusions in patients. (bloodjournal.org)
  • Vascular endothelial growth factor receptor 2 (VEGFR2) is highly expressed by lymphatic endothelial cells and has been shown to stimulate lymphangiogenesis in adult mice. (sigmaaldrich.com)
  • The VEGFs -A, -B, -C, -D are important signaling molecules with pivotal implication in the growth of blood and lymphatic vessels, the so-called angio- and lymphangiogenesis. (uib.no)
  • 4 The principal mechanism of these effects was initially thought to be the formation of new blood vessels by sprouting and migration of preexisting endothelial cells in ischemic tissue. (ahajournals.org)
  • Prognostic value of vascular endothelial growth factor expression in colorectal cancer patients. (labcorp.com)
  • Expression of vascular endothelial growth factor and its receptor, KDR, correlates with vascularity, metastasis, and proliferation of human colon cancer. (labcorp.com)
  • Combined analysis of vascular endothelial growth factor and platelet-derived endothelial cell growth factor expression in gastric carcinoma," International Journal of Cancer , vol. 74, no. 5, pp. 545-550, 1997. (hindawi.com)
  • observed in mouse that its expression was upregulated by hypoxia and that its cell surface receptor, Flk1, is exclusively expressed in endothelial cells. (lymphedemapeople.com)
  • Transcriptome analysis of hypervascularized islets revealed an increased expression of extracellular matrix components and axon guidance molecules, with these transcripts being enriched in the islet-derived endothelial cell population. (biologists.org)
  • 22.] Stavri GT, Zachary IC, Baskerville PA, Martin JF, Erusalimsky JD (1995) Basic fibroblast growth factor upregulates the expression of vascular endothelial growth factor in vascular smooth muscle cells. (thefreedictionary.com)
  • Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. (mdpi.com)
  • Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. (mdpi.com)
  • Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. (mdpi.com)
  • Upregulated expression of vascular endothelial growth factor in proliferative diabetic retinopathy. (bmj.com)
  • de Vries C, Escobedo JA, Ueno H, Houck K, Ferrara N, Williams LT (1992) The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor. (springer.com)
  • Terman BI, Dougher-Vermazen M, Carrion ME, Dimitrov D, Armellino DC, Gospodarowicz D, Bohlen P (1992) Identification of the KDR tyrosine kinase as a receptor for vascular endothelial cell growth factor. (springer.com)
  • 1997 ). Vascular endothelial growth factor up-regulates its receptor fms-like tyrosine kinase 1 (Flt-1) and a soluble variant of Flt-1 in human vascular endothelial cells. (biologists.org)
  • Schmidt A, Brixius K, Bloch W. Endothelial precursor cell migration during vasculogenesis. (springer.com)
  • 1997 ). Vascular endothelial growth factor stimulates tyrosine phosphorylation and recruitment to new focal adhesions of focal adhesion kinase and paxillin in endothelial cells. (biologists.org)
  • 2004 ) have also shown that overexpression of CYP4A1 in vascular smooth muscle cells promotes endothelial sprouting in renal arterial microvessels. (aspetjournals.org)
  • 5-8 However, extensive preclinical data have suggested that a portion of the effect of angiogenic cytokines (CKs) involves the mobilization and recruitment of precursor cells, capable of differentiation into endothelial cells, from the bone marrow (BM). (ahajournals.org)
  • This is the first reported case in Australia where intravitreal injections of anti-vascular endothelial growth factor ranibizumab were used to successfully. (ebscohost.com)
  • p38 signaling-mediated hypoxia-inducible factor 1 alpha and vascular endothelial growth factor induction by Cr(VI) in DU145 human prostate carcinoma cells. (cdc.gov)
  • Less is known about the cytokines responsible for generating the lymphatic vascular system. (rupress.org)
  • The proteinaceous milieu of malignant pleural effusions contains many growth factors and cytokines that may influence the dynamics of its formation. (aacrjournals.org)
  • The proliferation and growth of gastric cancer is mediated by a variety of growth factors and cytokines. (aacrjournals.org)
  • Hence, there has been recent interest in modifying the surface of platinum GDCs to promote thrombosis and endothelial cell proliferation, and thus reduce the time necessary for aneurysm occlusion (1-7) . (ajnr.org)
  • Vascular endothelial growth factor gene polymorphisms and idiopathic recurrent pregnancyloss. (thefreedictionary.com)
  • Background- We performed a series of investigations to test the hypothesis that combining angiogenic gene therapy and cytokine (CK)-induced endothelial progenitor cell mobilization would be superior to either strategy alone for treatment of chronic myocardial ischemia. (ahajournals.org)
  • The assembly of a functional vascular system requires a coordinated and dynamic transition from activation to maturation. (diva-portal.org)
  • Maturation involves junctional stabilization and formation of a functional endothelial barrier. (diva-portal.org)
  • However, the role VEGFR2 serves in the development of the lymphatic vascular system has not been defined. (sigmaaldrich.com)
  • Together, this work demonstrates that VEGFR2 directly promotes the expansion of the lymphatic network and further defines the molecular mechanisms controlling the development of the lymphatic vascular system. (sigmaaldrich.com)
  • 134920 ) and platelet-derived growth factors ( 173430 , 190040 ), are active on a wide range of different cell types. (lymphedemapeople.com)
  • It is, however, structurally related to platelet-derived growth factor. (lymphedemapeople.com)
  • These cDNAs encode hydrophilic proteins with sequences related to those of the A and B chains of platelet-derived growth factor. (sciencemag.org)
  • VEGFs are secreted proteins, in contrast to other endothelial cell mitogens such as acidic or basic fibroblast growth factors and platelet-derived endothelial cell growth factor. (sciencemag.org)
  • We also consider the effect of platelet-derived growth factor-B (PDGF-B) on the proliferation and migration of pericytes. (aimsciences.org)
  • Malignant pleural effusion formation is thought to be associated with high levels of these angiogenic proteins, and these high levels are thought to induce vascular permeability. (aacrjournals.org)
  • These data suggested that 20-HETE may induce angiogenic responses in endothelial cells (EC). (aspetjournals.org)
  • 1 It has been shown that capillarisation and phenotypic changes of the hepatic sinusoidal endothelial cells (SEC) occur during liver fibrosis development. (bmj.com)
  • Senger DR, Perruzzi CA, Feder J, Dvorak HF (1986) A highly conserved vascular permeability factor secreted by a variety of human and rodent tumor cell lines. (springer.com)
  • Association between vascular endothelial growth factor and hypertension in children and adolescents type I diabetes mellitus," Journal of Human Hypertension, vol. (thefreedictionary.com)
  • Up-regulation of endocrine gland-derived vascular endothelial growth factor but not vascular endothelial growth factor in human ectopic endometriotic tissue," Fertility and Sterility, vol. (thefreedictionary.com)
  • This genetic strategy initially induced a dense network of loosely adjoined endothelial cells and pericytes near lateral ventricles, similar to the immature vascular rete in human fetal brains. (sciencemag.org)
  • Similar effects occurred in 3 further types of human endothelial cell. (whiterose.ac.uk)
  • 1994 ). Spatial and temporal relationships between cadherins and PECAM-1 in cell-cell junctions of human endothelial cells. (biologists.org)
  • The relation between diabetes-associated increase in retinal AR activity and oxidative injury remains unexplored, and hyperglycemia-induced oxidative stress is present in cells with both relatively high (retinal pigment epithelial and Muller cells, pericytes) and low (endothelial cells) AR activity [( 19 ), R.N. Frank and A. Kennedy, unpublished]. (diabetesjournals.org)
  • Our findings indicate that Src can coordinate specific growth factor and extracellular matrix inputs by recruiting integrin αvβ5 into a FAK-containing signaling complex during growth factor-mediated biological responses. (rupress.org)
  • Prognostic significance of serum vascular endothelial growth factor per platelet count in unresectable advanced gastric cancer patients," Japanese Journal of Clinical Oncology , vol. 40, no. 12, Article ID hyq111, pp. 1147-1153, 2010. (hindawi.com)
  • Prognostic significance of serum levels of vascular endothelial growth factor and insulin-like growth factor-1 in advanced gastric cancer patients treated with FOLFOX chemotherapy," Chemotherapy , vol. 58, no. 6, pp. 426-434, 2012. (hindawi.com)
  • It is a ligand for VEGFR-1 (vascular endothelial growth factor receptor 1) and NRP-1 (neuropilin-1). (researchandmarkets.com)
  • An important growth factor receptor/ligand system implicated in gastric cancer progression is the epidermal growth factor (EGF) receptor (EGFR) and its ligands, EGF, transforming growth factor-α, and heparin binding EGF ( 11 , 12 ). (aacrjournals.org)
  • Bikfalvi A. (2017) Vascular Endothelial Growth Factor: The Cornerstone of Vascular Development Factors. (springer.com)
  • In the recent times, the global market for Global vascular endothelial growth factor inhibitor market research report 2017 has surfaced as one of the most promising markets in the pharmaceutical industry, thanks to the significant rise in research and development activities by leading vendors of Global vascular endothelial growth factor inhibitor market research report 2017 across the world. (qyresearchreports.com)
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  • The biology of vascular endothelial growth factor. (nih.gov)
  • Tammela T, Enholm B, Alitalo K, Paavonen K. The biology of vascular endothelial growth factors. (springer.com)