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.
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 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).
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 TIE receptor found predominantly on ENDOTHELIAL CELLS. It is considered essential for vascular development and can form a heterodimer with the TIE-2 RECEPTOR. The TIE-1 receptor may play a role in regulating BLOOD VESSEL stability and maturation.
A family of structurally-related tyrosine kinase receptors that are expressed predominantly in ENDOTHELIAL CELLS and are essential for development of BLOOD VESSELS (NEOVASCULARIZATION, PHYSIOLOGIC). The name derives from the fact that they are tyrosine kinases that contain Ig and EGF domains.
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.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
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.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
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.
A species of gram-negative bacteria highly pathogenic to RATS and MICE. It is the primary cause of murine respiratory mycoplasmosis.
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.
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 class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.
Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
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.
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.
Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina.
Glycoproteins found on the membrane or surface of cells.
The minute vessels that connect the arterioles and venules.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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.
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.
The blood vessels which supply and drain the RETINA.
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.
Agents and endogenous substances that antagonize or inhibit the development of new blood vessels.
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.
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.
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.
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.
Perforations through the whole thickness of the retina including the macula as the result of inflammation, trauma, degeneration, etc. The concept includes retinal breaks, tears, dialyses, and holes.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
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.
An area approximately 1.5 millimeters in diameter within the macula lutea where the retina thins out greatly because of the oblique shifting of all layers except the pigment epithelium layer. It includes the sloping walls of the fovea (clivus) and contains a few rods in its periphery. In its center (foveola) are the cones most adapted to yield high visual acuity, each cone being connected to only one ganglion cell. (Cline et al., Dictionary of Visual Science, 4th ed)
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
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.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
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.
Cell surface receptors that bind growth or trophic factors with high affinity, triggering intracellular responses which influence the growth, differentiation, or survival of cells.
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.
Removal of the whole or part of the vitreous body in treating endophthalmitis, diabetic retinopathy, retinal detachment, intraocular foreign bodies, and some types of glaucoma.
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.
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.
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.
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.
Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)
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.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
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.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
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.
Elements of limited time intervals, contributing to particular results or situations.
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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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).
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
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.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
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.
A cell line derived from cultured tumor cells.
Established cell cultures that have the potential to propagate indefinitely.

Molecular cloning and characterization of a novel angiopoietin family protein, angiopoietin-3. (1/589)

Using homology-based PCR, we have isolated cDNA encoding a novel member (491 amino acids) of the angiopoietin (Ang) family from human adult heart cDNA and have designated it angiopoietin-3 (Ang3). The NH2-terminal and COOH-terminal portions of Ang-3 contain the characteristic coiled-coil domain and fibrinogen-like domain that are conserved in other known Angs. Ang3 has a highly hydrophobic region at the N-terminus (approximately 21 amino acids) that is typical of a signal sequence for protein secretion. Ang3 mRNA is most abundant in adrenal gland, placenta, thyroid gland, heart and small intestine in human adult tissues. Additionally, Ang3 is a secretory protein, but is not a mitogen in endothelial cells.  (+info)

Angiopoietins 3 and 4: diverging gene counterparts in mice and humans. (2/589)

The angiopoietins have recently joined the members of the vascular endothelial growth factor family as the only known growth factors largely specific for vascular endothelium. The angiopoietins include a naturally occurring agonist, angiopoietin-1, as well as a naturally occurring antagonist, angiopoietin-2, both of which act by means of the Tie2 receptor. We now report our attempts to use homology-based cloning approaches to identify new members of the angiopoietin family. These efforts have led to the identification of two new angiopoietins, angiopoietin-3 in mouse and angiopoietin-4 in human; we have also identified several more distantly related sequences that do not seem to be true angiopoietins, in that they do not bind to the Tie receptors. Although angiopoietin-3 and angiopoietin-4 are strikingly more structurally diverged from each other than are the mouse and human versions of angiopoietin-1 and angiopoietin-2, they appear to represent the mouse and human counterparts of the same gene locus, as revealed in our chromosomal localization studies of all of the angiopoietins in mouse and human. The structural divergence of angiopoietin-3 and angiopoietin-4 appears to underlie diverging functions of these counterparts. Angiopoietin-3 and angiopoietin-4 have very different distributions in their respective species, and angiopoietin-3 appears to act as an antagonist, whereas angiopoietin-4 appears to function as an agonist.  (+info)

Angiopoietin-1 is an apoptosis survival factor for endothelial cells. (3/589)

We examined the effect of angiopoietin-1 (Ang1) on apoptosis in human umbilical vein endothelial cells (HUVECs). Ang1 (5-1000 ng/ml) dose-dependently inhibited apoptosis under a serum-deprived state. A significant apoptotic inhibition occurred with as low as 50 ng/ml. Two hundred ng/ml of Ang1 inhibited to approximately 50% of the control apoptotic rates for 96 h. Furthermore, an augmented antiapoptotic effect of Ang1 by the addition of 20 ng/ml vascular endothelial growth factor was observed. This Ang1-induced strong antiapoptotic effect in endothelial cells is a novel and intriguing finding and could be an additional description of Ang1-induced direct biological function.  (+info)

Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF. (4/589)

In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.  (+info)

The transcription factor MEF2C-null mouse exhibits complex vascular malformations and reduced cardiac expression of angiopoietin 1 and VEGF. (5/589)

The MEF2 family of transcription factors has been implicated in transcriptional regulation in a number of different cell types. Targeted deletion of the MEF2C gene, in particular, revealed its importance for early cardiogenesis (Q. Lin et al., 1997, Science 276, 1404-1407). We report here that this deletion also resulted in vascular anomalies characterized by extreme variability in lumen size and defects in remodeling. While primary vascular networks formed in the yolk sac of the mutants, they failed to remodel into more complex vascular structures. Likewise, although the primordia of the dorsal aortae formed normally, anomalies were observed in these vessels later in development. Dorsal and anterior to the heart, the aortae exhibited abnormally small lumens, as did the anterior cardinal veins and intersegmental arteries. In contrast, the dorsal aortae and intersegmental arteries caudal to the heart were grossly enlarged. Cranial vessels were also enlarged and less branched than normal. Endocardiogenesis in the mutant was abnormal with the endothelial cells exhibiting a number of aberrant phenotypes. These endocardial defects were accompanied by a notable reduction in angiopoietin 1 and VEGF mRNA production by the myocardium, indicating that MEF2C is required for myocardial expression of these important endothelial-directed cytokines and thus for correct endocardial morphogenesis.  (+info)

Expressions of angiopoietins and Tie2 in human choroidal neovascular membranes. (6/589)

PURPOSE: To elucidate the potential role of angiopoietins and the Tie2 system in choroidal neovascularization. METHODS: Surgically excised choroidal neovascular membranes (CNVMs) were obtained at vitrectomy from five eyes with age-related macular degeneration, three eyes with idiopathic neovascular maculopathy, and two eyes had degenerative myopia and two eyes had angioid streaks. Light microscopic immunohistochemistry was performed to detect cytokines such as vascular endothelial growth factor (VEGF), Ang1, and Ang2 and cellular components such as retinal pigment epithelial (RPE) cells, macrophages, and endothelial cells. Immunofluorescent double staining using confocal microscopy was performed to identify the cell types that secrete specific cytokines. RESULTS: Ang1 and Ang2 were positive in all surgically excised CNVMs, regardless of the primary disease. Double staining revealed that many of the cytokeratin, CD68 and factor VIII positive cells also had Ang1 and Ang2 immunoreactivities. In contrast to Ang1, Ang2 immunoreactivity tends to be higher in the highly vascularized regions of many CNVMs, and the localization was very similar to that of VEGF staining. Almost all vascular structures had prominent immunoreactivity for Tie2, which was confirmed by double staining for Tie2 and factor VIII. Tie2 immunoreactivity was also observed in the RPE monolayer and in pigmented, polygonal, and fibroblast-like cells in the stroma. CONCLUSIONS: Present findings that Ang2 and VEGF are co-upregulated and that Tie2 is expressed in a variety of cell types in CNVMs further support a crucial role of the interaction between VEGF and Ang2 in pathologic angiogenesis of CNVM formation.  (+info)

Expression of angiopoietin-1, angiopoietin-2, and the Tie-2 receptor tyrosine kinase during mouse kidney maturation. (7/589)

The Tie-2 receptor tyrosine kinase transduces embryonic endothelial differentiation, with Angiopoietin-1 (Ang-1) acting as a stimulatory ligand and Ang-2 postulated to be a naturally occurring inhibitor. Expression of these genes was sought during mouse kidney maturation from the onset of glomerulogenesis (embryonic day 14 [E14]) to the end of nephron formation (2 wk postnatal [P2]), and during medullary maturation into adulthood (P8). Using Northern and slot blotting of RNA extracted from whole organs, these three genes were expressed throughout the experimental period with peak levels at P2 to P3. By in situ hybridization analysis at E18, P1, and P3, Ang-1 mRNA was found to localize to condensing renal mesenchymal cells, proximal tubules, and glomeruli in addition to maturing tubules of the outer medulla. In contrast, Ang-2 transcripts were more spatially restricted, being detected only in differentiating outer medullary tubules and the vasa recta bundle area. Using in situ hybridization and immunohistochemistry, Tie-2 was detected in capillaries of the nephrogenic cortex, glomerular tufts, cortical interstitium, and medulla including vessels in the vasa recta. Using Western blotting of protein extracted from whole organs, Tie-2 protein was detected between E14 and P8 with tyrosine phosphorylated Tie-2 evident from E18. These data are consistent with the hypothesis that Tie-2 has roles in maturation of both glomeruli and vasa rectae.  (+info)

New model of tumor angiogenesis: dynamic balance between vessel regression and growth mediated by angiopoietins and VEGF. (8/589)

Our analyses in several different tumor settings challenge the prevailing view that malignancies and metastases generally initiate as avascular masses that only belatedly induce vascular support. Instead, we find that malignant cells rapidly co-opt existing host vessels to form an initially well-vascularized tumor mass. Paradoxically, the co-opted vasculature does not undergo angiogenesis to support the growing tumor, but instead regresses (perhaps as part of a normal host defense mechanism) via a process that involves disruption of endothelial cell/smooth muscle cell interactions and endothelial cell apoptosis. This vessel regression in turn results in necrosis within the central part of the tumor. However, robust angiogenesis is initiated at the tumor margin, rescuing the surviving tumor and supporting further growth. The expression patterns of Angiopoietin-2 (the natural antagonist for the angiogenic Tie2 receptor) and vascular endothelial growth factor (VEGF) strongly implicate these factors in the above processes. Angiopoietin-2 is highly induced in co-opted vessels, prior to VEGF induction in the adjacent tumor cells, providing perhaps the earliest marker of tumor vasculature and apparently marking the co-opted vessels for regression. Subsequently, VEGF upregulation coincident with Angiopoietin-2 expression at the tumor periphery is associated with robust angiogenesis. Thus, in tumors, Angiopoietin-2 and VEGF seem to reprise the roles they play during vascular remodeling in normal tissues, acting to regulate the previously underappreciated balance between vascular regression and growth.  (+info)

To test the hypothesis that the concentration of angiopoietin-2 relative to angiopoietin-1 may be a useful biological marker of mortality in acute lung injury patients. We also tested the association of concentration of angiopoietin-2 relative to ang
Angiopoietin-1/Tek signaling is a critical regulator of blood vessel development, with conventional knockout of angiopoietin-1 or Tek in mice being embryonically lethal due to vascular defects. In addition, angiopoietin-1 is thought to be required for the stability of mature vessels. Using a Cre-Lox conditional gene targeting approach, we have studied the role of angiopoietin-1 in embryonic and adult vasculature. We report here that angiopoietin-1 is critical for regulating both the number and diameter of developing vessels but is not required for pericyte recruitment. Cardiac-specific knockout of angiopoietin-1 reproduced the phenotype of the conventional knockout, demonstrating that the early vascular abnormalities arise from flow-dependent defects. Strikingly, deletion in the entire embryo after day E13.5 produced no immediate vascular phenotype. However, when combined with injury or microvascular stress, angiopoietin-1 deficiency resulted in profound organ damage, accelerated angiogenesis, ...
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TY - JOUR. T1 - Systemic analysis of tyrosine phosphorylated proteins in angiopoietin-1 induced signaling pathway of endothelial cells. AU - Kim, Young-Mee. AU - Seo, Jawon. AU - Yung, Hee Kim. AU - Jeong, Jaeho. AU - Hye, Joon Joo. AU - Lee, Dong Hee. AU - Gou, Young Koh. AU - Lee, Kong Joo. PY - 2007/8/1. Y1 - 2007/8/1. N2 - Angiogenesis is an essential process in physiological and pathological processes and is well-regulated to maintain the cellular homeostasis by balancing the endothelial cells in proliferation and apoptosis. Angiopoietin-1 (Ang1) regulates angiogenesis as a ligand of Tie 2 receptor tyrosine kinase. However, the regulation pathways are not well-understood. To date, only a few of the signaling molecules involved in the Tie 2 receptor tyrosine kinase-mediated angiogenesis have been identified. In this study, we systematically identified tyrosine-phosphorylated proteins in Ang1-induced signaling cascade in human umbilical vein endothelial cells (HUVECs), employing proteomic ...
TY - JOUR. T1 - Angiopoietin-1 protects endothelial cells from hypoxia-induced apoptosis via inhibition of phosphatase and tensin homologue deleted from chromosome ten. AU - Lee, Sae Won. AU - Youn, Seock Won. AU - Kim, Tae Youn. AU - Suh, Jung Won. AU - Koh, Gou Young. AU - Kwon, Yoo Wook. AU - Chae, In Ho. AU - Park, Young Bae. AU - Kim, Hyo Soo. PY - 2009/2. Y1 - 2009/2. N2 - Background and Objectives: Angiopoietin-1 (Ang1) is a regulator of blood vessel growth and maturation, and prevents radiation-induced or serum deprivation-induced apoptosis. Phosphatase and tensin homologue deleted from chromosome ten (PTEN), a well-known tumor suppressor, regulates cell cycle arrest and apoptosis. Hypoxia induces apoptosis by increasing the expression of PTEN. We hypothesized that Angl may regulate PTEN expression and, thus, reduce endothelial apoptosis under hypoxia in vitro and in vivo. Materials and Methods: In vitro, human umbilical vein endothelial cells (HUVECs) were treated with Ang1, and ...
The angiopoietin/Tie (ANG/Tie) receptor system controls developmental and tumor angiogenesis, inflammatory vascular remodeling, and vessel leakage. ANG1 is a Tie2 agonist that promotes vascular stabilization in inflammation and sepsis, whereas ANG2 is a context-dependent Tie2 agonist or antagonist. A limited understanding of ANG signaling mechanisms and the orphan receptor Tie1 has hindered development of ANG/Tie-targeted therapeutics. Here, we determined that both ANG1 and ANG2 binding to Tie2 increases Tie1-Tie2 interactions in a β1 integrin-dependent manner and that Tie1 regulates ANG-induced Tie2 trafficking in endothelial cells. Endothelial Tie1 was essential for the agonist activity of ANG1 and autocrine ANG2. Deletion of endothelial ...
Isolation of angiopoietin-1, a ligand for the TIE2 receptor, by secretion-trap expression cloning. The anticoagulation factor protein S and its relative, Gas6, are ligands for the Tyro 3/Axl family of receptor tyrosine kinases
TY - JOUR. T1 - Angiopoietin-2, permeability oedema, occurrence and severity of ALI/ARDS in septic and non-septic critically ill patients. AU - van der Heijden, M.. AU - van Nieuw Amerongen, G.P.. AU - Koolwijk, P.. AU - van Hinsbergh, V.W.M.. AU - Groeneveld, A.B.J.. PY - 2008. Y1 - 2008. U2 - 10.1136/thx.2007.087387. DO - 10.1136/thx.2007.087387. M3 - Article. C2 - 18559364. VL - 63. SP - 903. EP - 909. JO - Thorax. JF - Thorax. SN - 0040-6376. IS - 10. ER - ...
Effects of Protein and Gene Transfer of the Angiopoietin-1 Fibrinogen-like Receptor-binding Domain on Endothelial and Vessel ...
The results of the present study indicate that TAK1 acts as an AMPKα1 kinase in endothelial cells and positively regulates VEGF-induced, TNF-α-induced, and IL-1β-induced angiogenesis by increasing the expression of the antioxidative mitochondrial enzyme, SOD2. Indeed, superoxide production and the mitochondrial membrane potential were reduced in the absence of TAK1, and the impaired endothelial cell sprouting from aortic rings from TAKΔEC and AMPKα1ΔEC mice was rescued in the presence of PEG-SOD.. The global deletion of TAK1 impairs embryonic development in C. elegans,23 zebrafish, and mice.13 Both the global and endothelial-specific deletions of TAK1 result in vascular malformation, dilated capillaries, and defects in vascular stabilization,14 and correlate well with the phenotype of endothelial cell-specific TGF-β type II receptor conditional mutants.24 In addition to its role in vascular development, TAK1 has also been implicated in the TGF-β-induced regulation of matrix ...
In the circulatory system, while larger features of the vasculature such as arteries and veins appear to be statically positioned for years of use, finer features in the human body and in biology relates to a continuous branching out of a circulatory network that is required for tissue growth. This process is related to biochemical pathways and is vital to be understood so that issues in health and disease can be better addressed. Angiogenesis is the formation of new blood vessels from existing vessels. A functional vascular network is established by balanced angiogenesis processes. While the activation of angiogenesis extends vascular networks crucial for tissue growth, angiogenic vessels should be stabilized to undertake necessary vascular functions. The Notch pathway is fundamental for allowing for vascular stabilization. It acts by preventing excessive angiogenesis. However, how this signaling pathway that is conserved in various biological processes can induce changes that are ...
In this study we found that: (1) LS inhibits tubule formation in HUVECs and HMECs, but not BAECs, however CM from laminar sheared BAECs can inhibit tubule formation of HUVECs, (2) Preconditioning with LS inhibits migration in HUVECs and BAECs, whereas OS does not inhibit migration and this is mediated through secreted protein, (3) Ang2 is downregulated by LS both at the gene and protein level in vitro, (4) Ang2 is downregulated at sites of LS and upregulated at sites of OS in vivo, (5) Knockdown of Ang2 inhibits OS-mediated tubule formation and migration, and (6) Addition of recombinant Ang2 partially rescues LS-inhibited tubule formation. Collectively, these findings suggest that Ang2 secreted by ECs in response to OS, acts as a promigratory and proangiogenic molecule that could play an important role in diseases with altered shear stress.. Fluid shear stress is thought to play a role in angiogenesis and arteriogenesis. In angiogenesis, endothelial proliferation and migration are 2 important ...
The interaction between fluid status and angiopoietin-2 in adverse renal outcomes of chronic kidney disease. Yi-Chun Tsai, Yi-Wen Chiu, Hung-Tien Kuo, Jia-Jung Lee, Su-Chu Lee, Tzu-Hui Chen, Ming-Yen Lin, Shang-Jyh Hwang, Mei-Chuan Kuo, Ya-Ling Hsu, Hung-Chun Chen. Journal article , Research Article , Published 23 Mar 2017 , PLOS ONE ...
Looking for online definition of angiopoietin-2a in the Medical Dictionary? angiopoietin-2a explanation free. What is angiopoietin-2a? Meaning of angiopoietin-2a medical term. What does angiopoietin-2a mean?
TY - JOUR. T1 - Angiopoietin-1 regulates brain endothelial permeability through PTPN-2 mediated tyrosine dephosphorylation of occludin. AU - Siddiqui, M. Rizwan. AU - Mayanil, Chandra S.. AU - Kim, Kwang Sik. AU - Tomita, Tadanori. PY - 2015/6/19. Y1 - 2015/6/19. N2 - Objective Blood brain barrier (BBB) breakdown and increased endothelial permeability is a hallmark of neuro-vascular inflammation. Angiopoietin-1 (Ang-1), a Tie-2 receptor agonist ligand, is known to modulate barrier function of endothelial cells; however the molecular mechanisms related to Ang-1 mediated repair of Tight Junctions (TJs) in brain endothelium still remain elusive. In this study, we investigated a novel role of non-receptor protein tyrosine phosphatase N-2 (PTPN-2) in Ang-1 mediated stabilization of tight junction proteins. Method and Result To study the barrier protective mechanism of Ang-1, we challenged human brain microvascular endothelial cells in-vitro, with a potent inflammatory mediator thrombin. By using ...
Angiopoietins are a family of growth factors that are ligands for the tyrosine kinase receptor, Tie2. Angiopoietin 1 (Ang-1) is agonistic for Tie2, plays a key role in blood vessel maturation and stability and has been shown to possess anti-inflammatory properties. However, Tie2 expression has been demonstrated on human neutrophils and the observation that neutrophils migrate in response to Ang-1 in vitro has confounded research into its exact role in inflammation as well as its potential use as a therapeutic agent. We used a mouse model of peritoneal neutrophilic inflammation to determine if Ang-1 could stimulate neutrophil migration in vivo. Tie2 expression was demonstrated on mouse neutrophils. In addition, recombinant human Ang-1 induced significant chemotaxis of isolated mouse neutrophils in a Tie2- and CD18-dependent manner. Subsequently, co-immunoprecipitation of Ang-1 and CD18 demonstrated their interaction. Intraperitoneal injection of an engineered angiopoietin-1, MAT.Ang-1, induced ...
TY - JOUR. T1 - Coadministration of adenoviral vascular endothelial growth factor and angiopoietin-1 enhances vascularization and reduces ventricular remodeling in the infarcted myocardium of type 1 diabetic rats. AU - Mathews Samuel, Samson. AU - Akita, Yuzo. AU - Paul, Debayon. AU - Thirunavukkarasu, Mahesh. AU - Zhan, Lijun. AU - Sudhakaran, Perumana R.. AU - Li, Chuanfu. AU - Maulik, Nilanjana. PY - 2010/1/1. Y1 - 2010/1/1. N2 - OBJECTIVE - Hyperglycemia impairs angiogenesis in response to ischemia, leading to ventricular remodeling. Although the effects of overexpressing angiogenic growth factors have been studied in inducing angiogenesis, the formation of functional vessels remains a challenge. The present study evaluates the reversal of diabetes-mediated impairment of angiogenesis in the infarcted diabetic rat myocardium by proangiogenic gene therapy. RESEARCH DESIGN AND METHODS - Ad.VEGF and Ad.Ang1 were intramyocardially administered in combination immediately after myocardial ...
Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) play complementary roles in vascular development during embryogenesis. In the adult, VEGF signaling increases vascular permeability and Ang1 blocks this VEGF-mediated response. Gavard et al. provide evidence that this function of Ang1 is mediated by its actions on the endothelial cells, preventing them from responding to VEGF signaling that triggers disruption of adherens junctions. When injected subcutaneously in mice, Ang1 prevented dermal vascular permeability in response to VEGF injection (acute in vivo vascular permeability model). Experiments with cultured mouse endothelial cells revealed that Ang1 did not prevent VEGF from stimulating downstream effectors involved in proliferation (phosphorylation of Akt, extracellular signal-regulated kinases 1 and 2, and focal adhesion kinase) but did prevent disruption of endothelial barrier function by VEGF. Preexposure of endothelial cell cultures to Ang1 inhibited the ability of ...
TY - JOUR. T1 - Methylglyoxal modification of mSin3A links glycolysis to angiopoietin-2 transcription. AU - Yao, Dachun. AU - Taguchi, Tetsuya. AU - Matsumura, Takeshi. AU - Pestell, Richard. AU - Edelstein, Diane. AU - Giardino, Ida. AU - Suske, Guntram. AU - Ahmed, Naila. AU - Thornalley, Paul J.. AU - Sarthy, Vijay P.. AU - Hammes, Hans Peter. AU - Brownlee, Michael. PY - 2006/1/27. Y1 - 2006/1/27. N2 - Methylglyoxal is a highly reactive dicarbonyl degradation product formed from triose phosphates during glycolysis. Methylglyoxal forms stable adducts primarily with arginine residues of intracellular proteins. The biologic role of this covalent modification in regulating cell function is not known. Here, we report that in retinal Müller cells, increased glycolytic flux causes increased methylglyoxal modification of the corepressor mSin3A. Methylglyoxal modification of mSin3A results in increased recruitment of O-GlcNAc transferase to an mSin3A-Sp3 complex, with consequent increased ...
Angiopoietins and their receptor Tie-2 are, in concert with VEGF-A, key mediators in angiogenesis. This study evaluates the prognostic impact of all known human angiopoietins (Ang-1, Ang-2 and Ang-4) and their receptor Tie-2, as well as their relation to the prognostic expression of VEGF-A. 335 unselected stage I-IIIA NSCLC-patients were included and tissue samples of respective tumor cells and ...
This study demonstrates the distinct spatiotemporal expression profile of Angpt2 after MI and I/R, which, to date, has been obscure due to a lack of reliable antibodies (54). Using our recently developed anti-Angpt2 antibody (23), which is highly sensitive and specific to Angpt2, we demonstrate distinct expressions of Angpt2 on the ECs and proinflammatory macrophages after ischemia. This prompted us to further investigate the role of Angpt2 in postischemic cardiovascular remodeling. We recently reported that the FOXO1/Angpt2 axis suppresses the endothelial PI3K/Akt-signaling pathway, the main downstream pathway for Tie2 that plays a vital role in maintaining vascular integrity, inducing vascular destabilization in a positive feedback manner (25), and that it is central to the pathogenesis of sepsis (23), diabetic retinopathy (25), and tumor vessel destabilization (38). This study provides additional insights into the serious detrimental effects of the FOXO1/Angpt2 axis in exacerbating cardiac ...
Sphingosine-1-phosphate (S1P) is the endogenous ligand for the sphingosine-1-phophate receptors (S1P1-5) and triggers a number of cellular responses through their stimulation. S1P and its interaction with the S1P receptors play a significant role in a variety of biological processes including vascular stabilization, heart development, lymphocyte homing, and cancer angiogenesis. Agonism of S1P1, especially, has been shown to play an important role in lymphocyte trafficking from the thymus and secondary lymphoid organs, inducing immunosuppression, which has been established as a novel mechanism of treatment for immune diseases and vascular diseases. Sphingosine-1 -phosphate (SlP) has been demonstrated to induce many cellular effects, including those that result in platelet aggregation, cell proliferation, cell morphology, tumor cell invasion, endothelial cell and leukocyte chemotaxis, endothelial cell in vitro angiogenesis, and lymphocyte trafficking. SlP receptors are therefore good targets for a ...
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Rabbit polyclonal Angiopoietin 1 + Angiopoietin 2 antibody. Validated in WB, ICC/IF and tested in Rat, Human. Cited in 14 publication(s). Immunogen corresponding to synthetic peptide.
To investigate the theory, Bhandari and colleagues first tested a cohort of lung secretion samples taken from premature infants. After testing the samples, the researchers found that miR-34a was significantly increased only in the samples taken from babies who went on to develop BPD. The researchers also tested lung tissue collected postmortem from babies who had died at different ages from lung disease. Again, they found that this particular microRNA was expressed in the samples and also its downstream targets (the production of proteins) were suppressed in the ones with BPD. Next, the researchers found that levels of miR-34a levels were increased in the lungs of neonatal mice exposed to high levels of oxygen. Bhandari and his team then blocked the microRNA by repressing gene expression, as well as pharmacologically, by injecting the mouse models with the downstream target of the miR-34a, angiopoietin-1. Blocking miR-34a or injecting angiopoietin-1 in the mouse models improved their lung ...
Meet us at the ASBMR in Orlando at The Biomedica booth # 516 Our Posters: #SUN-103, #SUN-271, #MON-252 and #MON-331 Tje Bone Turnover Markers Working Group Room# W307B, Sept 20 at 7:30pm Diurnal Changes in Serum Levels of Bone-Related Circulating MicroRNAs. Oral presentation #1140, room# W314, Monday, Sept 23 from 2:15pm-2:30pm If you cannot make it to the ASBMR ...
The ANGPT-TIE2 pathway is important for angiogenesis, lymphangiogenesis and inflammation, and therefore has important roles in cancer. Given the context-dependent and opposing effects of the ANGPTs, how do we target this pathway? Angiopoietins (ANGPTs) are ligands of the endothelial cell receptor TIE2 and have crucial roles in the tumour angiogenic switch. Increased expression of ANGPT2 relative to ANGPT1 in tumours correlates with poor prognosis. The biological effects of the ANGPT-TIE system are context dependent, which brings into question what the best strategy is to target this pathway. This Review presents an encompassing picture of what we know about this important axis in tumour biology. The various options for
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Polyclonal antibody for Angiopoietin 2/ANGPT2 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: IHC-P. Reactive species: Human. Angiopoietin 2/ANGPT2 information: Molecular Weight: 56919 MW; Subcellular Localization: Secreted.
Yn aml mae gan enynnau lawer o gyfystyron. Mae hyn oherwydd eu bod yn aml yn cael eu darganfod gan nifer o bobl mewn cyd-destunau gwahanol heb wybod mair un genynnau oeddyn nhw. Hefyd mae gan wahanol gymunedau gwyddonol safonau gwahanol ar gyfer enwi genynnau. Dyma restr o gyfystyron ar gyfer y genyn ANGPT2. ...
Affiliation:名古屋市立大学,大学院医学研究科,講師, Research Field:Ophthalmology, Keywords:脈絡膜新生血管,炎症,加齢黄斑変性,ペリサイト,細胞生物学,リポフスチン,Angiopoietin-2,マウス,発現抑制,脂質, # of Research Projects:5, # of Research Products:33, Ongoing Project:加齢黄斑変性の病態におけるブルッフ膜への加齢性沈着脂質の役割の解明
Angiopoietin 2 antibody (angiopoietin 2) for ELISA, IHC-P, WB. Anti-Angiopoietin 2 pAb (GTX10601) is tested in Human samples. 100% Ab-Assurance.
Angiopoietin 1兔多克隆抗体(ab94684)可与小鼠, 人样本反应并经WB, IHC实验严格验证并得到1个独立的用户反馈。所有产品均提供质保服务,中国75%以上现货。
Published data on the role of the Ang/tie-2 system in cardiovascular diseases are limited. Most of our knowledge regarding the angiopoietins has come from oncology studies where angiogenesis is a prerequisite for tumor growth and metastasis. Indeed, Ang-2 has been shown to be a marker of a poor prognosis in breast cancer and non-small cell lung cancer (4,21). In the present paper, we describe a new assay for Ang-1 and, in addition, have demonstrated (for the first time in the literature) very abnormal levels of Ang-2 and tie-2, but normal Ang-1, in CHF. Vascular endothelial growth factor was marginally raised in the patients, suggesting that Ang-2 may be more relevant to the pathophysiology of this disease. In addition, there was a significant correlation between Ang-2 and tie-2.. That Ang-1 is not raised in CHF is consistent with currently held views that its secretion is not stimulated by hypoxia, as demonstrated in animal studies (13,14,22). Angiopoietin-1 has been shown to have antiapoptotic ...
Background: Microcirculatory dysfunction is associated with multiple organ failure and unfavorable patient outcome. We investigated whether therapeutically targeting the endothelial angiopoietin/Tie2 system preserves microvascular integrity during hemorrhagic shock. Methods: Rats were treated with the angiopoietin-1 mimetic vasculotide and subjected to hemorrhagic shock and fluid resuscitation. Microcirculatory perfusion and leakage were assessed with intravital microscopy (n = 7 per group) and Evans blue dye extravasation (n = 8 per group), respectively. The angiopoietin/Tie2 system was studied at protein and RNA level in plasma, kidneys, and lungs. Results: Hemorrhagic shock significantly reduced continuously perfused capillaries (7 ± 2 vs. 11 ± 2) and increased nonperfused vessels (9 ± 3 vs. 5 ± 2) during hemorrhagic shock, which could not be restored by fluid resuscitation. Hemorrhagic shock increased circulating angiopoietin-2 and soluble Tie2 significantly, which associated with ...
Angiopoietin-related protein 2 also known as angiopoietin-like protein 2 is a protein that in humans is encoded by the ANGPTL2 gene. Angiopoietin-like protein 2 maintains tissue homeostasis by promoting adaptive inflammation and subsequent tissue reconstruction, whereas an excess of ANGPTL2 activation induced by prolonged stress promotes the breakdown of tissue homeostasis due to chronic inflammation, promoting the development of metabolic diseases. ANGPTL2 has a role also in angiogenesis, in tissue repair, in obesity, in atherosclerotic diseases and finally in cancerogenesis. Angiopoietins are members of the vascular endothelial growth factor family and the only known growth factors largely specific for vascular endothelium. Angiopoietin-1, angiopoietin-2, and angiopoietin-4 participate in the formation of blood vessels. ANGPTL2 protein is a secreted glycoprotein with homology to the angiopoietins and may exert a function on endothelial cells through autocrine or paracrine action. GRCh38: ...
Notch and Angiopoietin-1 (Ang1)/Tie2 pathways are crucial for vascular maturation and stability. Here we identify the transcription factor ERG as a key regulator of endothelial Notch signalling. We show that ERG controls the balance between Notch ligands by driving Delta-like ligand 4 (Dll4) while repressing Jagged1 (Jag1) expression. In vivo, this regulation occurs selectively in the maturing plexus of the mouse developing retina, where Ang1/Tie2 signalling is active. We find that ERG mediates Ang1-dependent regulation of Notch ligands and is required for the stabilizing effects of Ang1 in vivo. We show that Ang1 induces ERG phosphorylation in a phosphoinositide 3-kinase (PI3K)/Akt-dependent manner, resulting in ERG enrichment at Dll4 promoter and multiple enhancers. Finally, we demonstrate that ERG directly interacts with Notch intracellular domain (NICD) and {beta}-catenin and is required for Ang1-dependent {beta}-catenin recruitment at the Dll4 locus. We propose that ERG coordinates Ang1, ...
Background. In sepsis and various other inflammatory conditions, elevated circulating levels of angiopoietin-2 (Ang2) are detected, but the precise functional role of Ang2 in these conditions is not well understood. Here, we investigated the contribution of Ang2 to the inflammatory response and renal function impairment in a mouse model of endotoxaemia.. Methods. Ang2-deficient mice and wild-type littermates were challenged with lipopolysaccharide [LPS; 1500 EU/g, intraperitoneal (i.p.)]. In additional experiments, wild-type C57Bl/6 mice were depleted of circulating neutrophils by antibody treatment (NIMPR14) prior to LPS challenge to study the role of neutrophils in regulating LPS-induced cytokine release. After 8 or 24 h of LPS challenge, the mice were sacrificed and organs were harvested. Quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay were performed for endothelial adhesion molecules (P-selectin, E-selectin, VCAM-1 and ICAM-1) and plasma ...
Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or therapeutic agent is available. Here we show that lung micro-RNA (miR)-34a levels are significantly increased in lungs of neonatal mice exposed to hyperoxia. Deletion or inhibition of miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-34a overexpression. Administration of angiopoietin-1, which is one of the downstream targets of miR34a, is able to ameliorate the BPD pulmonary and PAH phenotypes. Using three independent cohorts of human samples, we show that miR-34a expression is increased in type 2 alveolar epithelial cells in neonates with respiratory distress syndrome and BPD. Our data suggest that pharmacologic miR-34a inhibition may be a therapeutic option to prevent or ameliorate HALI/BPD in neonates.
Mice. Specific pathogen-free (SPF) C57BL/6J mice (catalog 000664), Tie2-GFP mice (catalog 003658), and UBC-Cre-ERT2 mice (catalog 007001) were purchased from the Jackson Laboratory. Angpt1fl/fl mice were a gift from Yoshikazu Nakaoka (Osaka University, Osaka, Japan), Angpt1-GFP mice were a gift from Sean J. Morrison (University of Texas Southwestern, Dallas, Texas, USA), Angpt2-lacZ mice were a gift from Nicholas Gale (Regeneron Pharmaceuticals), and Vegfr2fl/fl mice were a gift from Masanori Hirashima (Kobe University, Kobe, Japan). Prox1-GFP (30), Angpt1-GFP (33), Prox1fl/fl (39), Tie2fl/fl (35), Angpt1fl/fl (36, 37), Angpt2fl/fl (38), Vegfr2fl/fl (55), and Angpt2-lacZ (22) mice were transferred and bred in our SPF animal facility at KAIST. To deplete Prox1, Tie2, or Vegfr2 genes specifically in ECs, VE-cadherin-Cre-ERT2 mice (34) were mated with either Prox1fl/fl, Tie2fl/fl, or Vegfr2fl/fl mice to obtain EC-specific Prox1-, Tie2-, or Vegfr2-deleted mice, respectively, in a tamoxifen-dependent ...
Human platelet lysate (PL) is a cost-effective and human source of autologous multiple and potent pro-angiogenic factors, such as vascular endothelial growth factor A (VEGF A), fibroblast growth factor b (FGF b) and angiopoietin-1. Nanocoatings previously characterized were prepared by layer-by-layer assembling incorporating PL with marine-origin polysaccharides and were shown to activate human umbilical vein endothelial cells (HUVECs). Within 20 h of incubation, the more sulfated coatings induced the HUVECS to the form tube-like structures accompanied by an increased expression of angiogenic-associated genes, such as angiopoietin-1 and VEGF A. This may be a cost-effective approach to modify 2D/3D constructs to instruct angiogenic cells towards the formation of neo-vascularization, driven by multiple and synergistic stimulations from the PL combined with sulfated polysaccharides.. ...
ENCODES a protein that exhibits identical protein binding (ortholog); INVOLVED IN animal organ regeneration (ortholog); liver regeneration (ortholog); negative regulation of apoptotic process (ortholog); PARTICIPATES IN angiopoietin signaling pathway; ASSOCIATED WITH brain ischemia (ortholog); Diabetes Mellitus, Experimental (ortholog); diabetic retinopathy (ortholog); FOUND IN extracellular space (inferred); integral component of membrane (inferred); membrane raft (inferred)
Purified Recombinant Human ANGPT1/COMP protein, FLAG-tagged from Creative Biomart. Recombinant Human ANGPT1/COMP protein, FLAG-tagged can be used for research.
401366DNAHomo sapiens 1gaggtgcagc tggtggagtc tgggggaggc ttggtccagc ctggggggtc cctgagactc 60tcctgtgcag tctctggatt cacctttagt agctattgga tgagctgggt ccgccaggct 120ccagggaagg ggctggagtg ggtggccaac ataaagcaag atggaagtga gaaatactat 180gtggactctg tgaagggccg attcaccatc tccagagaca acgccaagaa ctcactgtat 240ctgcaaatga acagcctgag agccgaggac acggctgtgt attactgtgc gagagatcaa 300ggtatagcag tggctgggcc ctttgactac tggggccagg gaaccctggt caccgtctcc 360tcagcc 3662122PRTHomo Sapiens 2Glu Val Gln Leu Val Glu Ser Gly Gly Gly Leu Val Gln Pro Gly Gly1 5 10 15Ser Leu Arg Leu Ser Cys Ala Val Ser Gly Phe Thr Phe Ser Ser Tyr 20 25 30Trp Met Ser Trp Val Arg Gln Ala Pro Gly Lys Gly Leu Glu Trp Val 35 40 45Ala Asn Ile Lys Gln Asp Gly Ser Glu Lys Tyr Tyr Val Asp Ser Val 50 55 60Lys Gly Arg Phe Thr Ile Ser Arg Asp Asn Ala Lys Asn Ser Leu Tyr65 70 75 80Leu Gln Met Asn Ser Leu Arg Ala Glu Asp Thr Ala Val Tyr Tyr Cys 85 90 95Ala Arg Asp Gln Gly Ile Ala Val Ala Gly Pro Phe Asp Tyr Trp Gly 100 105 110Gln Gly Thr Leu Val Thr Val Ser ...
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Explore the angiopoietin-TIE2 signaling pathway and find antibodies to detect some of its target proteins, including CD202b (TIE2), AKT, ERK1, and ERK2.
ANGPT2 (Human) ELISA Kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human ANGPT2. (KA1867) - Products - Abnova
Detect and quantitate human angiopoietin 1 (ANGPT1) in buffered solution and cell culture supernatants using a homogeneous LANCE Ultra TR-FRET assay.
Camenisch G et al. (2002) ANGPTL3 stimulates endothelial cell adhesion and migration via integrin alpha vbeta 3 and induces blood vessel formation in vivo.. [^] ...
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Utilization of cylindrical roller linear guide that up-level the parallelism between molds, and improve the cleanless circumstance around mold by lubrication-free on tie bar for its guider function has been replaced. ...
AGPT2 - Angpt2 - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector shRNA available for purchase from OriGene - Your Gene Company.

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