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 layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.
Single layer of large flattened cells covering the surface of the cornea.
Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces.
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.
Adherence of cells to surfaces or to other cells.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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.
The main trunk of the systemic arteries.
The nonstriated involuntary muscle tissue of blood vessels.
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.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)
The minute vessels that connect the arterioles and venules.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
The vessels carrying blood away from the heart.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
Cell adhesion molecule and CD antigen that mediates neutrophil, monocyte, and memory T-cell adhesion to cytokine-activated endothelial cells. E-selectin recognizes sialylated carbohydrate groups related to the Lewis X or Lewis A family.
Drugs used to cause dilation of the blood vessels.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
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)
Drugs used to cause constriction of the blood vessels.
White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
That phase of a muscle twitch during which a muscle returns to a resting position.
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 layer of the cornea. It is the basal lamina of the CORNEAL ENDOTHELIUM (from which it is secreted) separating it from the CORNEAL STROMA. It is a homogeneous structure composed of fine collagenous filaments, and slowly increases in thickness with age.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
Movement of tethered, spherical LEUKOCYTES along the endothelial surface of the microvasculature. The tethering and rolling involves interaction with SELECTINS and other adhesion molecules in both the ENDOTHELIUM and leukocyte. The rolling leukocyte then becomes activated by CHEMOKINES, flattens out, and firmly adheres to the endothelial surface in preparation for transmigration through the interendothelial cell junction. (From Abbas, Cellular and Molecular Immunology, 3rd ed)
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 collect blood from the capillary plexuses and join together to form veins.
The veins and arteries of the HEART.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
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.
Partial or total replacement of the CORNEA from one human or animal to another.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
Bipotential angio-hematopoietic stem cells that give rise to both HEMATOPOIETIC STEM CELLS and ENDOTHELIAL CELLS.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
A purely physical condition which exists within any material because of strain or deformation by external forces or by non-uniform thermal expansion; expressed quantitatively in units of force per unit area.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Microscopy in which the object is examined directly by an electron beam scanning the specimen point-by-point. The image is constructed by detecting the products of specimen interactions that are projected above the plane of the sample, such as backscattered electrons. Although SCANNING TRANSMISSION ELECTRON MICROSCOPY also scans the specimen point by point with the electron beam, the image is constructed by detecting the electrons, or their interaction products that are transmitted through the sample plane, so that is a form of TRANSMISSION ELECTRON MICROSCOPY.
Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
An essential amino acid that is physiologically active in the L-form.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Endothelial cells that line venous vessels of the UMBILICAL CORD.
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.
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
Cell adhesion molecule and CD antigen that serves as a homing receptor for lymphocytes to lymph node high endothelial venules.
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.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
The passage of cells across the layer of ENDOTHELIAL CELLS, i.e., the ENDOTHELIUM; or across the layer of EPITHELIAL CELLS, i.e. the EPITHELIUM.
The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.
Antibodies produced by a single clone of cells.
Elements of limited time intervals, contributing to particular results or situations.
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.
Integrin alpha4beta1 is a FIBRONECTIN and VCAM-1 receptor present on LYMPHOCYTES; MONOCYTES; EOSINOPHILS; NK CELLS and thymocytes. It is involved in both cell-cell and cell- EXTRACELLULAR MATRIX adhesion and plays a role in INFLAMMATION, hematopoietic cell homing and immune function, and has been implicated in skeletal MYOGENESIS; NEURAL CREST migration and proliferation, lymphocyte maturation and morphogenesis of the PLACENTA and HEART.
Transmembrane proteins consisting of a lectin-like domain, an epidermal growth factor-like domain, and a variable number of domains that are homologous to complement regulatory proteins. They are important cell adhesion molecules which help LEUKOCYTES attach to VASCULAR ENDOTHELIUM.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP.
The vessels carrying blood away from the capillary beds.
The carbohydrate-rich zone on the cell surface. This zone can be visualized by a variety of stains as well as by its affinity for lectins. Although most of the carbohydrate is attached to intrinsic plasma membrane molecules, the glycocalyx usually also contains both glycoproteins and proteoglycans that have been secreted into the extracellular space and then adsorbed onto the cell surface. (Alberts et al., Molecular Biology of the Cell, 3d ed, p502)
A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.
The finer blood vessels of the vasculature that are generally less than 100 microns in internal diameter.
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
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.
Treatment process involving the injection of fluid into an organ or tissue.
A system of organs and tissues that process and transport immune cells and LYMPH.
A competitive inhibitor of nitric oxide synthetase.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
Direct contact of a cell with a neighboring cell. Most such junctions are too small to be resolved by light microscopy, but they can be visualized by conventional or freeze-fracture electron microscopy, both of which show that the interacting CELL MEMBRANE and often the underlying CYTOPLASM and the intervening EXTRACELLULAR SPACE are highly specialized in these regions. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p792)
Disorder caused by loss of endothelium of the central cornea. It is characterized by hyaline endothelial outgrowths on Descemet's membrane, epithelial blisters, reduced vision, and pain.
The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.
A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.
The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
An integrin heterodimer widely expressed on cells of hematopoietic origin. CD11A ANTIGEN comprises the alpha chain and the CD18 antigen (ANTIGENS, CD18) the beta chain. Lymphocyte function-associated antigen-1 is a major receptor of T-CELLS; B-CELLS; and GRANULOCYTES. It mediates the leukocyte adhesion reactions underlying cytolytic conjugate formation, helper T-cell interactions, and antibody-dependent killing by NATURAL KILLER CELLS and granulocytes. Intracellular adhesion molecule-1 has been defined as a ligand for lymphocyte function-associated antigen-1.
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
Diseases of the cornea.
An excessive amount of fluid in the cornea due to damage of the epithelium or endothelium causing decreased visual acuity.
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.
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 strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
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 flow of BLOOD through or around an organ or region of the body.
Cell surface glycoproteins on lymphocytes and other leukocytes that mediate adhesion to specialized blood vessels called high endothelial venules. Several different classes of lymphocyte homing receptors have been identified, and they appear to target different surface molecules (addressins) on high endothelial venules in different tissues. The adhesion plays a crucial role in the trafficking of lymphocytes.
A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.
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 ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
The innermost layer of the heart, comprised of endothelial cells.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
The state of activity or tension of a muscle beyond that related to its physical properties, that is, its active resistance to stretch. In skeletal muscle, tonus is dependent upon efferent innervation. (Stedman, 25th ed)
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.
Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.
Veins which return blood from the intestines; the inferior mesenteric vein empties into the splenic vein, the superior mesenteric vein joins the splenic vein to form the portal vein.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Centers for storing various parts of the eye for future use.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
A form of fluorescent antibody technique commonly used to detect serum antibodies and immune complexes in tissues and microorganisms in specimens from patients with infectious diseases. The technique involves formation of an antigen-antibody complex which is labeled with fluorescein-conjugated anti-immunoglobulin antibody. (From Bennington, Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
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.
Tubular vessels that are involved in the transport of LYMPH and LYMPHOCYTES.
A layer of the peritoneum which attaches the abdominal viscera to the ABDOMINAL WALL and conveys their blood vessels and nerves.
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 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.
The lamellated connective tissue constituting the thickest layer of the cornea between the Bowman and Descemet membranes.
Diseases, dysfunctions, or disorders of or located in the iris.
Family of proteins associated with the capacity of LEUKOCYTES to adhere to each other and to certain substrata, e.g., the C3bi component of complement. Members of this family are the LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; (LFA-1), the MACROPHAGE-1 ANTIGEN; (Mac-1), and the INTEGRIN ALPHAXBETA2 or p150,95 leukocyte adhesion protein. They all share a common beta-subunit which is the CD18 antigen. All three of the above antigens are absent in inherited LEUKOCYTE-ADHESION DEFICIENCY SYNDROME, which is characterized by recurrent bacterial infections, impaired pus formation, and wound healing as well as abnormalities in a wide spectrum of adherence-dependent functions of granulocytes, monocytes, and lymphoid cells.
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.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
The process by which a tissue or aggregate of cells is kept alive outside of the organism from which it was derived (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
The arterial blood vessels supplying the CEREBRUM.
The artery formed by the union of the right and left vertebral arteries; it runs from the lower to the upper border of the pons, where it bifurcates into the two posterior cerebral arteries.
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
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.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Relatively complete absence of oxygen in one or more tissues.
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.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
Established cell cultures that have the potential to propagate indefinitely.
The clear, watery fluid which fills the anterior and posterior chambers of the eye. It has a refractive index lower than the crystalline lens, which it surrounds, and is involved in the metabolism of the cornea and the crystalline lens. (Cline et al., Dictionary of Visual Science, 4th ed, p319)
A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
Glycoproteins found on the membrane or surface of cells.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The internal resistance of a material to moving some parts of it parallel to a fixed plane, in contrast to stretching (TENSILE STRENGTH) or compression (COMPRESSIVE STRENGTH). Ionic crystals are brittle because, when subjected to shear, ions of the same charge are brought next to each other, which causes repulsion.
Methods of maintaining or growing biological materials in controlled laboratory conditions. These include the cultures of CELLS; TISSUES; organs; or embryo in vitro. Both animal and plant tissues may be cultured by a variety of methods. Cultures may derive from normal or abnormal tissues, and consist of a single cell type or mixed cell types.
The vein which drains the foot and leg.
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
The main artery of the thigh, a continuation of the external iliac artery.
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 group of three different alpha chains (CD11a, CD11b, CD11c) that are associated with an invariant CD18 beta chain (ANTIGENS, CD18). The three resulting leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE ADHESION) are LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; MACROPHAGE-1 ANTIGEN; and ANTIGEN, P150,95.
The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)
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.
A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)
The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and VISCOSITY.
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.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
The circulation of the BLOOD through the LUNGS.
A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
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.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.
An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.
A tyrosine phosphoprotein that plays an essential role in CAVEOLAE formation. It binds CHOLESTEROL and is involved in LIPIDS transport, membrane traffic, and SIGNAL TRANSDUCTION.
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).

VEGF is required for growth and survival in neonatal mice. (1/25855)

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)

Primary haemostasis: sticky fingers cement the relationship. (2/25855)

Platelet aggregation to form a haemostatic plug, or thrombus, plays a key role in preventing bleeding from a wound. Recent studies have provided new insights into how platelet receptors are deployed during the interactions with the vascular subendothelial matrix that lead to haemostatic plug formation.  (+info)

Bcl-2 and Bcl-XL serve an anti-inflammatory function in endothelial cells through inhibition of NF-kappaB. (3/25855)

To maintain the integrity of the vascular barrier, endothelial cells (EC) are resistant to cell death. The molecular basis of this resistance may be explained by the function of antiapoptotic genes such as bcl family members. Overexpression of Bcl-2 or Bcl-XL protects EC from tumor necrosis factor (TNF)-mediated apoptosis. In addition, Bcl-2 or Bcl-XL inhibits activation of NF-kappaB and thus upregulation of proinflammatory genes. Bcl-2-mediated inhibition of NF-kappaB in EC occurs upstream of IkappaBalpha degradation without affecting p65-mediated transactivation. Overexpression of bcl genes in EC does not affect other transcription factors. Using deletion mutants of Bcl-2, the NF-kappaB inhibitory function of Bcl-2 was mapped to bcl homology domains BH2 and BH4, whereas all BH domains were required for the antiapoptotic function. These data suggest that Bcl-2 and Bcl-XL belong to a cytoprotective response that counteracts proapoptotic and proinflammatory insults and restores the physiological anti-inflammatory phenotype to the EC. By inhibiting NF-kappaB without sensitizing the cells (as with IkappaBalpha) to TNF-mediated apoptosis, Bcl-2 and Bcl-XL are prime candidates for genetic engineering of EC in pathological conditions where EC loss and unfettered activation are undesirable.  (+info)

Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages. (4/25855)

Both chlamydial and human heat shock protein 60s (HSP 60), which colocalize in human atheroma, may contribute to inflammation during atherogenesis. We tested the hypothesis that chlamydial or human HSP 60 activates human endothelial cells (ECs), smooth muscle cells (SMCs), and monocyte-derived macrophages. We examined the expression of adhesion molecules such as endothelial-leukocyte adhesion molecule-1 (E-selectin), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), and the production of the proinflammatory cytokine interleukin-6 (IL-6). We also tested whether either HSP 60 induces nuclear factor-kappaB (NF-kappaB), which contributes to the gene expression of these molecules. Either chlamydial or human HSP 60 induced E-selectin, ICAM-1, and VCAM-1 expression on ECs similar to levels induced by Escherichia coli lipopolysaccharide (LPS). Each HSP 60 also significantly induced IL-6 production by ECs, SMCs, and macrophages to an extent similar to that induced by E. coli LPS, as assessed by enzyme-linked immunosorbent assay (ELISA). In ECs, either HSP 60 triggered activation of NF-kappaB complexes containing p65 and p50 Rel proteins. Heat treatment abolished all these effects, but did not alter the ability of E. coli LPS to induce these functions. Chlamydial and human HSP 60s therefore activate human vascular cell functions relevant to atherogenesis and lesional complications. These findings help to elucidate the mechanisms by which a chronic asymptomatic chlamydial infection might contribute to the pathophysiology of atheroma.  (+info)

Role of alphavbeta3 integrin in the activation of vascular endothelial growth factor receptor-2. (5/25855)

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. (6/25855)

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)

Novel endotheliotropic herpesviruses fatal for Asian and African elephants. (7/25855)

A highly fatal hemorrhagic disease has been identified in 10 young Asian and African elephants at North American zoos. In the affected animals there was ultrastructural evidence for herpesvirus-like particles in endothelial cells of the heart, liver, and tongue. Consensus primer polymerase chain reaction combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and another in African elephants. Otherwise healthy African elephants with external herpetic lesions yielded herpesvirus sequences identical to that found in Asian elephants with endothelial disease. This finding suggests that the Asian elephant deaths were caused by cross-species infection with a herpesvirus that is naturally latent in, but normally not lethal to, African elephants. A reciprocal relationship may exist for the African elephant disease.  (+info)

Endothelial cells modulate the proliferation of mural cell precursors via platelet-derived growth factor-BB and heterotypic cell contact. (8/25855)

Embryological data suggest that endothelial cells (ECs) direct the recruitment and differentiation of mural cell precursors. We have developed in vitro coculture systems to model some of these events and have shown that ECs direct the migration of undifferentiated mesenchymal cells (10T1/2 cells) and induce their differentiation toward a smooth muscle cell/pericyte lineage. The present study was undertaken to investigate cell proliferation in these cocultures. ECs and 10T1/2 cells were cocultured in an underagarose assay in the absence of contact. There was a 2-fold increase in bromodeoxyuridine labeling of 10T1/2 cells in response to ECs, which was completely inhibited by the inclusion of neutralizing antiserum against platelet-derived growth factor (PDGF)-B. Antisera against PDGF-A, basic fibroblast growth factor, or transforming growth factor (TGF)-beta had no effect on EC-stimulated 10T1/2 cell proliferation. EC proliferation was not influenced by coculture with 10T1/2 cells in the absence of contact. The cells were then cocultured so that contact was permitted. Double labeling and fluorescence-activated cell sorter analysis revealed that ECs and 10T1/2 cells were growth-inhibited by 43% and 47%, respectively. Conditioned media from contacting EC-10T1/2 cell cocultures inhibited the growth of both cell types by 61% and 48%, respectively. Although we have previously shown a role for TGF-beta in coculture-induced mural cell differentiation, growth inhibition resulting from contacting cocultures or conditioned media was not suppressed by the presence of neutralizing antiserum against TGF-beta. Furthermore, the decreased proliferation of 10T1/2 cells in the direct cocultures could not be attributed to downregulation of the PDGF-B in ECs or the PDGF receptor-beta in the 10T1/2 cells. Our data suggest that modulation of proliferation occurs during EC recruitment of mesenchymal cells and that heterotypic cell-cell contact and soluble factors play a role in growth control during vessel assembly.  (+info)

Trelagliptin, an oral DPP-4 inhibitor, which is administered once per week and characterized by a long half-life in blood. The effects of trelagliptin on vascular endothelial functions have not been clarified to date. The objective of the present study was to examine the effects of trelagliptin on vascular endothelial functions in patients with type 2 diabetes mellitus (DM) using flow-mediated dilatation (FMD), adiponectin, and asymmetric dimethylarginine (ADMA) as evaluation indicators. This study was a preliminary single-arm prospective pilot study. The subjects of this study were type 2 DM patients aged 20-74 years, who visited our outpatient department. The patients were treated with trelagliptin, and their FMD, adiponectin, and ADMA levels were measured at baseline and at 12 weeks after initial treatment to determine the changes during the study period. A total of 27 patients, excluding three dropouts, were included in the population for analysis. Trelagliptin treatment showed no significant
This study will investigate the effects of vildagliptin compared with glimepiride on vascular endothelial function in patients with type 2 diabetes mellitus.
This study investigated the effect of sitagliptin and vildagliptin (DPP-4 Inhibitor) on vascular endothelial function in Type 2 Diabetes Mellitus patients.
TY - JOUR. T1 - Endothelial cell seeding on crosslinked collagen: effects of crosslinking on endothelial cell proliferation and functional parameters. AU - Wissink, M.J.B.. AU - van Luijn, M.J.A.. AU - Beernink, R.. AU - Dijk, F.. AU - Poot, A.A.. AU - Engbers, G.H.M.. AU - Beugeling, T.. AU - van Aken, W.G.. AU - Feijen, J.. PY - 2000. Y1 - 2000. N2 - Endothelial cell seeding, a promising method to improve the performance of small-diameter vascular grafts, requires a suitable substrate, such as crosslinked collagen. Commonly used crosslinking agents such as glutaraldehyde and formaldehyde cause, however, cytotoxic reactions and thereby hamper endothelialization of currently available collagen-coated vascular graft materials.The aim of this study was to investigate the effects of an alternative method for crosslinking of collagen, using N-(3-dimethylaminopropyl)-N-ethylcarbodiimide (EDC) in combination with N-hydroxysuccinimide (NHS), on various cellular functions of human umbilical vein ...
TY - JOUR. T1 - Vascular endothelium. AU - Daugherty, M. O.. AU - Rich, G. F.. AU - Johns, R. A.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - Our understanding of the vital function of the vascular endothelium in circulatory physiology is rapidly expanding. Endothelium-derived vasoactive substances influence vascular tone, growth, inflammation, and haemostasis. Endothelial dysfunction is implicated in the pathophysiology of cardiovascular diseases such as atherosclerosis, ischaemia-reperfusion injury, hypertension, and congestive heart failure. New pharmacological therapies are evolving from our understanding of the role of the endothelium.. AB - Our understanding of the vital function of the vascular endothelium in circulatory physiology is rapidly expanding. Endothelium-derived vasoactive substances influence vascular tone, growth, inflammation, and haemostasis. Endothelial dysfunction is implicated in the pathophysiology of cardiovascular diseases such as atherosclerosis, ischaemia-reperfusion injury, ...
To the best of our knowledge, the present study is the largest to compare the effect on endothelial function, assessed by FMD, of different types of exercise training in post-myocardial infarction patients. Several interesting findings emerged from our trial.. First, in accordance with previous reports,19,24 an important degree of endothelial dysfunction (assessed by FMD) was found in a large, homogeneous group of patients 3 weeks after an acute myocardial infarction. In fact, the mean percent FMD was significantly inferior (4.2%) to a value considered normal in healthy subjects (≈10%).22. Second, in line with previous results,7,19 exercise helped to restore endothelial function as shown by the improvement in indexes of systemic endothelial function in all trained patients, whereas no significant changes in endothelium-independent vasodilatation were apparent. This adaptation appears to be predominantly endothelium dependent9; in fact, exercise increases shear stress, which is a strong ...
Endothelial cell dysfunction has been extensively associated with hypercholesterolemia and atherogenesis. However, most of the early work relevant to endothelial vascular function has focused on large conduit vessels (eg, the aorta, iliac arteries, large coronary arteries, etc), which are common sites of atherosclerotic lesions but are not generally involved in the direct regulation of tissue perfusion. Conversely, the microvasculature regulates tissue perfusion but does not usually develop overt atherosclerosis. Nevertheless, studies of the microvascular endothelium may be of importance in assessing the overall cardiovascular effect of atherosclerosis because it may represent an early marker of atherogenesis. Thus, endothelial function may be abnormal in this segment of the circulation, despite the absence of lesions in larger vessels in the setting of hyperlipidemia and atherosclerosis. In the present article, we have shown that 1-week administration of a 0.5% cholesterol diet to rabbits ...
Aging stem cells may play a critical role in determining the effects of aging on organ function. With regard to vascular diseases, it has been postulated that circulating EPCs are involved in the repair mechanisms after endothelial damage (27,28). Ultimately, deterioration of endothelial or vascular function may be related to both quantitative and qualitative changes of stem cells.. We describe here the first comprehensive analysis of the association between age-related endothelial dysfunction and the number and function of circulating EPCs, defined by expression of CD34+/VEGFR2+ and CD133+/VEGFR2+. Although no quantitative differences in EPCs were observed, our data illustrate that culture-enriched EPCs from old but otherwise healthy subjects are impaired in terms of fundamental functional features like proliferation (important for amplifying the cellular pool), migration (critical for homing of circulating EPCs), and survival. We demonstrate a significant univariate correlation between the ...
Our work identifies AMPKα1 as a new kinase that phosphorylates Ser188 of RhoA and establishes a novel signaling cascade induced by estradiol. In VSMC, ER stimulation by E2 activates AMPK that phosphorylates RhoA thereby reducing Rho-Rock signaling pathway activity and limiting vasoconstriction. Our results also demonstrate that AMPKα1-RhoA pathway is constitutively active in female mice and could thus participate to the vasoprotective effect of estrogens.. AMPK is an ubiquitous heterotrimeric serine/threonine protein kinase activated by pathological stimuli, such as oxidative damage, osmotic shock, hypoxia, and glucose deprivation, as well as by physiological stimuli such as exercise and muscle contraction, and by hormones including leptin and adiponectin.27 In general, AMPK is activated in response to decreased cellular energy charge (increased in AMP/ATP ratio) and regulates carbohydrate and lipid metabolism.28-30 Although there is a robust correlation between the activity of the AMPK and ...
The endothelium serves as one of the main targets of the SARS-CoV-2 virus, and endothelial dysfunction largely determines the pathogenesis and clinical outcome in COVID-19 (Teuwen et al., 2020). Pathophysiological studies demonstrated inflammatory activation of the endothelium, destruction of intercellular contacts, and disruption of contacts with the basement membrane in COVID-19 (Ackermann et al., 2020). Dysfunction of the endothelium, apparently, was one of the reasons for thrombosis, both of the pulmonary capillaries and deep veins. At the same time, there was a significant stimulation of angiogenesis (Teuwen et al., 2020), which was caused by damage to the endothelium and hypoxia in the affected areas of the lung. Signs of viral infection of endothelial cells were found not only in the vessels of the lungs, but also in the heart and other organs, and were also confirmed in vitro using a model of vascular organoids (Monteil et al., 2020). Mitochondria in endothelial cells do not play a large role in
Definition of endothelial-derived relaxant factor in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is endothelial-derived relaxant factor? Meaning of endothelial-derived relaxant factor as a legal term. What does endothelial-derived relaxant factor mean in law?
Fingerprint Entra nei temi di ricerca di (AS) TNF-alpha blockade induces a reversible but transient effect on endothelial dysfunction in patients with long-standing severe rheumatoid arthritis.. Insieme formano una fingerprint unica. ...
UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
Fingerprint Dive into the research topics of Mathematical modeling of vascular endothelial cell layer maintenance: the role of endothelial cell division, progenitor cell homing and telomere shortening. Together they form a unique fingerprint. ...
The study of endothelial cells has provided unique insight into important cardiovascular diseases and the control of angiogenesis during tumour development. The control of new blood vessel formation, or angiogenesis, is orchestrated by vascular endothelium and endothelial cells respond to unique signals in their environment with a repertoire of cellular and molecular responses. Studies directed towards dissecting the molecular mechanisms underlying alterations in genotype and phenotype are underway using prototypic endothelial cell gene products (e.g. endothelin-1, eNOS, CXCR4, adhesion molecules such as VCAM-1 or ICAM-1) and exciting models of cellular activation (hypoxia, shear stress and epigenetic modifiers). An excellent example of the applicability of this approach is our finding that shigatoxins, bacterial-derived exotoxins that cause severe inflammation of capillary beds in patients with E coli 0157:H7, regulate the expression of genes in vascular endothelium at the post-transcriptional ...
This prospective study demonstrated that impaired FMD of the brachial artery is a strong independent predictor of cardiovascular events in patients with peripheral arterial disease. The predictive value of FMD was independent of the extent of reactive hyperemia and the response to an exogenous source of nitric oxide (NTG), suggesting that the findings are not due to variation in the stimulus for vasodilation or the function of vascular smooth muscle. Thus, the study supports a pathophysiologic link between endothelial dysfunction and cardiovascular events.. Previous invasive coronary studies examined the relation between endothelial dysfunction and cardiovascular risk. During a 28-month follow-up of 157 patients, Suwaidi et al. (3)demonstrated that coronary endothelial dysfunction in the absence of obstructive lesions was associated with increased cardiovascular events. Schachinger et al. (4)reported that impaired vasodilator responses to both endothelium-dependent and -independent agonists ...
Clinical assessment of endothelial function involves the measurement of dilation of conductance arteries during periods of acute increases in shear stress, believed to be almost entirely mediated by NO release, or measurement of agonist-induced vasodilation.1-3 The magnitude of endothelial dysfunction is an important and independent predictor of future development of cardiovascular risk factors, such as hypertension and diabetes, and of cardiovascular events.4-8 Thus, assessment of endothelial function quantifies subclinical vascular damage and is a valuable prognostic tool.3,4 The available clinical techniques for estimating endothelial function require substantial expertise and are not suitable for use in routine clinical practice. There is, thus, a critical need for simpler tests, potentially biomarkers, that would provide an accurate index of vascular endothelial function.. The bioavailability of NO from the vascular endothelium is exquisitely modulated by reactive oxygen species that ...
OBJECTIVE--To assess a non-invasive test for endothelial dysfunction, an important early event in the atherogenic process. METHODS--Using high resolution ultrasound, the accuracy of detecting small changes in vessel diameter was assessed using phantom arteries, and the same equipment was then used to measure flow mediated dilatation in the brachial artery of 40 healthy adults aged 22-51 years, studied on four occasions; intervals between scans were 1-2 days, 1-2 weeks, and 2-4 months. RESULTS--Differences between pairs of phantom arteries with diameters 0.1-0.2 mm apart were correctly estimated in 162 of 264 cases (61%); no measurement by any of four independent observers was , 0.1 mm in error, and the mean error was 0.04 mm. For in vivo scans, the overall coefficient of variation for flow mediated dilatation was 1.8% (1.6% for women, 1.9% for men, P = 0.18). In 34/40 subjects (85%), all values for flow mediated dilatation were within 2.5% of the overall mean for each subject. A nested ...
Endothelium plays a critical role in maintaining healthy homeostatic properties of the vasculature. Endothelial dysfunction promotes atherosclerosis by creating a vasospastic, prothrombotic, and proinflammatory milieu. Therefore, the assessment of endothelial function as a surrogate marker of arterial health has gained significant interest for clinical risk assessment beyond the risk conveyed by a structural impediment to flow (1). Furthermore, the observation that cardiovascular events may occur remotely from the site in which the endothelial dysfunction is detected prompted clinical studies in search for peripheral vascular endothelial dysfunction as a predictor of cardiovascular events.. Endothelial dysfunction is characterized by a paradoxical vasoconstriction or attenuated dilation due to reduced endothelium-dependent nitric oxide (NO) release. In earlier studies, the response of the epicardial arteries to infused acetylcholine was measured invasively to assess endothelial function in the ...
The endothelium is the lining of our arteries and consists of a single layer of tile-like cells. The endothelium is central to artery health and disease. Anything that compromises the health of the endothelium has an immediate effect on the flow of blood to every organ. Atherosclerosis, the obstruction of arteries by cholesterol, is merely the end result of repeated endothelial damage. Every fat and cholesterol laden meal causes an inflammatory storm within the arteries that lasts for many hours and has a measureable effect on endothelial function.. Endothelial cells are continually releasing nitric oxide and many other chemical messengers that control blood flow and blood clotting. Nitric oxide (NO) is the key player. It diffuses into the muscular layer of the artery wall and causes the muscle cells to relax a little. The physics of pipes and fluids dictates that a small increase in the diameter of the vessel results in a big increase in blood flow. This provides for minute to minute adjustment ...
Ventricular hypertrophy following chronic overload results from the hypertrophy of cardiomyocytes and the hyperplasia of non muscle cells in the
Endothelial dysfunction has been implicated in the pathological process of coronary artery disease as well as an adverse event after coronary drug eluting stent (DES) implantation. In this review, an overview will be given of the evidence to date regarding the effects of coronary DES on endothelial function obtained from both clinical and experimental studies. Stenting in general and DES seem to impair several aspects of endothelial function: provision of a permeable barrier function; modulation of adhesion, thrombosis and inflammation; and regulation of vascular tone. However, new insights show that the effects of DES can extend beyond the stent and peri-stent area: the vascular bed distal to the stent, starting with the distal conduit vessels up to the distal microvasculature, might be at risk. In addition, insight into the mechanism of DES induced endothelial dysfunction has been gained. To finalize this review, clinical complications and solutions of DES associated endothelial dysfunction ...
Background: Water pipe (WP) tobacco smoking is gaining wide popularity among young and middle aged males and females. Aim of the work: The aim of this study was to evaluate the immediate effect of 1st pipe water smoking on brachial Flow mediated dilatation% (FMD%) and Nitrate mediated dilatation% (NMD%) as markers of systemic endothelial function. Methods:...
Vascular endothelium is responsible for the secretion of several substances exerting anti-atherogenic effects. Endothelial damage is also crucial for the progress of atherosclerosis and risk factors for atherosclerosis represent crucial factors associated with endothelial dysfunction. Studies have shown that patients with cardiovascular disease are characterized by impaired endothelial function (EF). Therefore, several agents have been proposed as potential modulators of EF. Most of the available approaches include pharmaceutical agents routinely used such as statins, angiotensin converting enzyme inhibitors, antioxidants, L-arginine, insulin sensitizers or others still under investigation such as tetrahydrobiopterin or folic acid (folate). Despite of the fact that there are several strategies aiming to improve endothelial dysfunction by enhancing nitric oxide bioavailability, it is still unclear whether they could be beneficial at a clinical level.
There are several invasive and noninvasive methods available to the clinical researcher for the assessment of endothelial function. The first investigations in humans involved invasive pharmacological vascular function testing, which have been used to gain a detailed understanding of the mechanisms involved in the pathogenesis of endothelial dysfunction and atherosclerosis as well as novel targets for intervention. Techniques for endothelial function testing have evolved over time from these invasive methods, which, by their nature, are restricted to small studies in the research laboratory, to more standardized noninvasive methods, which are suitable for use in large prospective cohort studies and clinical trials. This paper describes currently available methods for assessment of endothelial function and their potential application in cardiovascular research and clinical practice.
Background: While diabetes is associated with diminished vascular NO levels, the precise mechanisms of diabetic endothelial dysfunction are not known. We hypothesized that deficient eNOS S1179 phosphorylation plays a key role in diabetic vascular abnormalities, and that increasing S1179 phosphorylation may improve endothelial function. To test this hypothesis, we created eNOS knock-in mice that carry a S1179D mutation in the eNOS gene, resulting in the generation of a phosphomimetic form of eNOS with increased enzymatic activity and NO generation. We bred these animals to db/db mice to obtain S1179D-db/db mice to test whether modulation of the S1179 phosphorylation site could overcome diabetic vascular dysfunction, and whether this could affect stroke size in vivo.. Experimental Procedures: Adult male mice were anesthetized by 30 % oxygen, 70 % nitrous oxide, and 1.5 % isoflurane. Body temperature was maintained at 36-37°C. Vessel reactivity studies were performed on isolated pressurized ...
TY - JOUR. T1 - Effect of diet on vascular reactivity. T2 - an emerging marker for vascular risk.. AU - West, S. G.. PY - 2001/11. Y1 - 2001/11. N2 - New technology for studying vascular activity in vivo has shown that the endothelium plays a critical role in the development of atherosclerosis. The healthy endothelium is a metabolically active tissue that exquisitely regulates vascular tone via release of the powerful vasodilator, nitric oxide. Endothelial integrity reduces cell adhesion, lipid deposition, and other early steps in atherogenesis. There is compelling evidence that endothelial function can be altered within hours of eating certain foods, further affirming the role of dietary factors in the prevention and progression of cardiovascular disease. This article reviews recent work on dietary factors (fatty acids, L-arginine, antioxidants, polyphenols, and folic acid) that alter vascular tone, and critically evaluates two noninvasive measures (flow-mediated dilation and total peripheral ...
The results of our prospective study clearly demonstrate that endothelial function significantly influences the future development of diabetes, independently of age and several other well-known diabetes risk factors. In our opinion, this is a very important tool because it radically changes the way endothelial dysfunction is considered. Endothelial dysfunction is usually explained as being the consequence of the endothelium being exposed to damaging factors, e.g., high blood pressure, high cholesterol, high blood glucose, smoking, etc.-the response-to-injury theory (3). Our data revolutionize the concept because they indicate that endothelial dysfunction may influence the development of diabetes. The present results have been obtained by studying a population of postmenopausal women who represent a unique model of studying endothelial dysfunction consequences. In fact, the decrease in estrogens that physiologically follows menopause does in itself compromise the endothelial function in women, ...
Were stained with rat endothelial cell antigen. + pixels were counted in glomeruli and tubular fields working with ImageJ Application . To be able to evaluate
Vascular endothelium provides a selective barrier between the blood and tissues, participates in wound healing and angiogenesis, and regulates tissue recruitment of inflammatory cells. Nuclear factor (NF)- \(\kappa\)B transcription factors are pivotal regulators of survival and inflammation, and have been suggested as potential therapeutic targets in cancer and inflammatory diseases. Here we show that mice lacking IKK\(\beta\), the primary kinase mediating NF-\(\kappa\)B activation, are smaller than littermates and born at less than the expected Mendelian frequency in association with hypotrophic and hypovascular placentae. IKK\(\beta\) -deleted endothelium manifests increased vascular permeability and reduced migration. Surprisingly, we find that these defects result from loss of kinase-independent effects of IKK\(\beta\) on activation of the serine-threonine kinase, Akt. Together, these data demonstrate essential roles for IKK\(\beta\) in regulating endothelial permeability and migration, as ...
Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of the adhesion receptor Gpr116/ADGRF5 has remained elusive. We generated a new mouse model of constitutive Gpr116 inactivation, with a large genetic deletion encompassing exon 4 to exon 21 of the Gpr116 gene. This model allowed us to confirm recent results defining Gpr116 as necessary regulator of surfactant homeostasis. The loss of Gpr116 provokes an early accumulation of surfactant in the lungs, followed by a massive infiltration of macrophages, and eventually progresses into an emphysemalike pathology. Further analysis of this knockout model revealed cerebral vascular leakage, beginning at around 1.5 months of age. Additionally, endothelial-specific deletion of Gpr116 resulted in a significant increase of the brain vascular leakage. Mice devoid of Gpr116 developed an anatomically normal and largely functional vascular network, surprisingly exhibited an attenuated ...
vascular protection contains many products you can buy at the lowest price at VitaZita. Ordering from the category vascular protection is quick and easy.
vascular protection contains many products you can buy at the lowest price at VitaZita. Ordering from the category vascular protection is quick and easy.
The thin layer of cells that lines the interior of blood vessels, known as the endothelium, plays a complex role in vascular biology. The endothelium mediates blood vessel tone, hemostasis, neutrophil recruitment, hormone trafficking, and fluid filtration. Endothelial dysfunction, as defined by a lack of NO, has been linked to a variety of disease states, including atherosclerosis, diabetes mellitus, coronary artery disease, hypertension, and hypercholesterolemia. Indeed, restoration of endothelial function is one of the earliest recognizable benefits of statin therapy. In 1995, James Liao and colleagues published a study in the ...
A discovery arose from growing human arterial endothelial cells in the lab, and scientists from the Morgridge Institute for Research couldn’t be more
The present invention relates to intercellular adhesion inhibitory factors produced by cytokine activated endothelial cells. These factors designated endothelial-derived IL-8 find use in the diagnosis and treatment of inflammation and in the protection of endothelial cells from neutrophil mediated damage.
In normal vascular physiology, nitric oxide (NO) plays a key role in maintaining the vascular wall in a quiescent state by inhibition of inflammation, cellular proliferation, and thrombosis (1). What is generally referred to as endothelial dysfunction should more appropriately be considered endothelial activation. Such activation may be beneficial to humans in certain instances, such as during infection, and harmful in others, such as during obesity.. During infection, a reduction in NO may allow for activation of endothelial expression of chemokines, cytokines, and adhesion molecules, designed to recruit and activate leukocytes and platelets. Endothelial activation (endothelial dysfunction) may be considered as a beneficial and physiological response to infection.. In the absence of an active infection, most cardiovascular risk factors (smoking, elevated lipids, hypertension, aging) reduce NO bioavailability-a maladaptive response that sets the stage for the development of atherosclerosis. The ...
My laboratory is interested in bi-directional crosstalk between vascular endothelium and cardiomyocytes that regulates cardiac size and function. As an alternative to myocyte-driven hypertrophy in response to hemodynamic stress we recently reported a cross-talk loop induction of myocardial hypertrophy by expanding vascular endothelium in the absence of traditional hypertrophy stimuli. This reveals a new and unexplored role played by the endothelium in regulation of adult organ growth and size that would be of great interest in formulating new therapeutic angiogenic approaches to the treatment of heart disease.. Our hypothesis is that an increase in vascular endothelium in the adult heart results in increased nitric oxide (NO) production that in turn drives the growth of cardiomyocytes by sustained ubiquitination of the negative regulator of G protein signaling subtype 4 (RGS4) and derepression of the hypertrophic program via heterotrimeric G protein signaling. To investigate this crosstalk we ...
Endothelium helps in maintaining vascular tone by regulating the vascular permeability. It selectively allows only certain molecules to cross the endothelial barrier. A large number of micro and macro vascular complications are associated with endothelial dysfunction in diabetes including cardiovascular disease, stroke and peripheral vascular diseases. Moreover, a series of
Fingerprint Dive into the research topics of Evidence for vasculoprotective effects of ET,sub,B,/sub, receptors in resistance artery remodeling in diabetes. Together they form a unique fingerprint. ...
1) The rate of NO release from endothelial cells increases when flow is enhanced. (2) Endothelial cells possess a high capacity for NO production, permitting a rapid adjustment of NO release to changes in flow. (3) The rate of NO release is not causally related to changes in perfusion pressure ...
The vascular endothelium comprises a dynamic interface with the blood and acts as an integrator and transducer of both biochemical (e.g. inflammatory cytokines)...
When the endothelial cells get affected, the walls of the arteries tend to lose their elasticity thereby becoming hard and thick. Many studies in the cardiovascular field point out that endothelial dysfunction is the clinical manifestation of cardiovascular disease.
Ease of Ang-2 from endothelia is mediated by Tlr4 [13] and we JI 101 site detected mRNA levels of Tlr4 on HUVECs (Figure 6A). Prior studies have shown that
Endothelial dysfunction has been shown to be of significance in predicting stroke and heart attacks due to the inability of the arteries to dilate fully.
Fatma Aykas, Yalcin Solak, Abdulsamet Erden, Kadir Bulut, Selcuk Dogan, Bahadır Sarli, Gokhan Acmaz, Baris Afsar, Dimitrie Siriopol, Adrian Covic, Shailendra Sharma, Richard J. Johnson, Mehmet Kanbay ...
Diabetes mellitus leads to endothelium dysfunction and an accelerated progression of atherosclerosis. Vascular complications of diabetes mellitus can affect not only large and medium arteries resulting in coronary heart disease and peripheral arteries diseases, but also small vessels leading to retinopathy and nephropathy. Intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin and von Willebrand factor (vWF) are considered as markers of endothelium dysfunction. The aim of our study was to evaluate plasma levels of ICAM-1, VCAM-1, E-selectin and vWF in patients with type 2 diabetes mellitus receiving insulin therapy and who had diabetic non-proliferative retinopathy, proliferative retinopathy, or did not develop diabetic retinopathy. There were no statistically significant differences between studied groups in any of evaluated endothelium dysfunction markers. There was no statistically significant correlation between measured parameters and a period of ...
TY - JOUR. T1 - Endothelium removal augments endothelium-independent vasodilatation in rat mesenteric vascular bed. AU - Iwatani, Y.. AU - Kosugi, K.. AU - Isobe-Oku, S.. AU - Atagi, S.. AU - Kitamura, Yoshihisa. AU - Kawasaki, H.. PY - 2008/5. Y1 - 2008/5. N2 - Background and purpose: The vascular endothelium regulates vascular tone by releasing various endothelium-derived vasoactive substances to counteract excess vascular response. We investigated whether the vascular endothelium regulates vasodilatation via released endothelium-derived contracting factors (EDCFs), by examining the effect of endothelium removal on responses to periarterial nerve stimulation (PNS) and various vasodilator agents. Experimental approach: The rat mesenteric vascular bed was perfused with Krebs solution. Vasodilator responses to PNS and 5 min perfusion of vasodilator agents in preparations with endothelium were compared with those in the same preparations without endothelium. The endothelium was removed by 30 s ...
During inflammation, neutrophils migrate from the vascular lumen into extravascular sites. In vitro assays have suggested that platelet-endothelial cell adhesion molecule-1 [PECAM-1 (CD31)], a member of the immunoglobulin superfamily, is required for the transmigration of neutrophils across endothelial monolayers. Antibody to human PECAM-1, which cross-reacts with rat PECAM-1, was found to block not only in vivo accumulation of rat neutrophils into the peritoneal cavity and the alveolar compartment of the lung but also neutrophil accumulation in human skin grafts transplanted onto immunodeficient mice. On the basis of these findings in three different models of inflammation, it appears that PECAM-1 is required for neutrophil transmigration in vivo and may thus be a potential therapeutic target. ...
Atrial natriuretic peptide (ANP), a hormone considered to be an important regulator of intravascular fluid volume, has been shown to bind specifically to receptors on endothelial cells. In this study, the role of ANP-specific binding was investigated by examining the effect of ANP on the morphology and macromolecular permeability of monolayer cultures of bovine aortic endothelial cells (BAEC). ANP alone (10-9 -10-6 M) had no observable effect on the morphology of the monolayers. However, incubation of the endothelial monolayers with ANP (10-8 -10-6 M) antagonized the characteristic thrombin-induced (1 unit/ml) cell shape changes and the formation of intercellular gaps. Since chemically and enzymatically generated oxidants have also been shown to alter endothelial cell shape and increase macromolecular permeability, the effect of ANP on oxidant-induced injuries was investigated. Treatment of endothelial monolayers with glucose oxidase (1.4 unit/ml) elicited changes in cell shape characterized by ...
TY - JOUR. T1 - Regulation of vascular endothelial barrier function by Epac, a cAMP-activated exchange factor for Rap GTPase. AU - Cullere, Xavier. AU - Shaw, Sunil K.. AU - Andersson, Lorna. AU - Hirahashi, Junichi. AU - Luscinskas, Francis W.. AU - Mayadas, Tanya N.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - Endothelial cell-cell junctional proteins and cortical actin are of central importance for regulating vascular permeability. Rap1, a member of the Ras family of GTPases, is enriched at endothelial cell-cell contacts and activated by cyclic AMP (cAMP) through a PKA-independent pathway. Activation of a cAMP-inducible gua nine-exchange factor for Rap, Epac, results in markedly enhanced basal endothelial barrier function by increasing cortical actin and subsequent redistribution of adherens and tight junctional molecules to cell-cell contacts. Activation of Epac also counteracts thrombin-induced hyperpermeability through down-regula tion of Rho GTPase activation, suggesting cross-talk between Rap and ...
The adherence and migration of leukocytes through the endothelium of blood vessels is an important early event which occurs in normal tissues following ionizing irradiation but the underlying mechanisms are not fully understood. ICAM-1, VCAM-1 and CD31 are membrane proteins of endothelial cells, mediate this process when the vasculature is exposed to other inflammatory stimuli. In this study, expression of ICAM-1, VCAM-1 and CD31 on human dermal microvascular endothelial cells (HDMECs) at 72 hours post-irradiation using flow cytometry and northern analysis was determined. Dose-dependent increases in the surface expression and mRNA of ICAM-1 and CD31 were observed. In contrast VCAM-1 was practically undetectable on both control and irradiated HDMECs but was strongly expressed in TNF-alpha activated positive control HDMECs. The upregulation in ICAM-1 and CD31 was independent of radiation-induced changes in cell size, number and cell cycle stage. We suggest that ICAM-1 is active over a prolonged ...
TY - JOUR. T1 - Thrombin-induced gap formation in confluent endothelial cell monolayers in vitro. AU - Laposata, Michael. AU - Dovnarsky, D. K.. AU - Shin, H.. PY - 1983. Y1 - 1983. N2 - When thrombin is incubated with confluent monolayers of human umbilical vein endothelial cells in vitro, there is a change in the shape of the endothelial cells that results in gaps in the monolayer disrupting the integrity of the endothelium and exposing the subendothelium. Using a grid assay to measure this phenomenon, we observed that up to 80% of the surface area once covered by cells was uncovered after a 15-min incubation with 10-2 U/ml (10-10 M) thrombin. The effect was apparent within 2 min and did not remove cells from the surface of the culture dish. The gaps in the monolayer completely disappeared within 2 hr after exposure to thrombin. The effect of thrombin was inhibited by preincubation of thrombin with hirudin or antithrombin III plush heparin or by preincubation of the monolayers with dibutyryl ...
Endothelial activation is an integral component of inflammatory rheumatic diseases, and also of atherosclerosis. Leukocytes emigrate from the blood into inflamed tissues through a series of adhesion events (the adhesion cascade), each of which is dependent upon the state of endothelial cell activation. Initial rolling of neutrophils on vascular endothelium is mediated by transient interactions between selectins (L-selectin on leukocytes, E-selectin on cytokine-activated endothelial cells (EC) and P-selectin on both activated EC and activated platelets) and carbohydrate-bearing counter-structures on the opposing cell. Whilst rolling, leukocytes become exposed to activating signals (such as chemokines), resulting in an upregulation of the capacity of b2 integrins (eg LFA-1, Mac-1) to bind ligands (eg ICAM-1, -2) on EC. This integrin-mediated secondary adhesion results in leukocyte arrest and is followed by their transmigration into the tissues. In the case of mononuclear cells, adhesion of a4 ...
Statins Nonlipid Effects on Vascular Endothelium through eNOS Activation Curator, Author,Writer, Reporter: Larry Bernstein, MD, FACP Categories of Research: Disease biology, Cell Biology and Cell Signaling, Biological Networks and Gene Regulation, Pharmacotherapy of Cardiovascular Disease, Nitric Oxide, HMG Co A inhibitors, Endothelial Receptor, Hypertension, Therapeutic Targets Introduction Statins have an effect on the…
HIV infected patients treated with abacavir might have a higher risk for the occurrence of cardiovascular events. At time of writing of this protocol the underlying mechanism is not yet elucidated, however some studies find impaired endothelial function and elevated markers of chronic inflammation in these patients,suggesting a higher lever of chronic inflammation. Recently maraviroc (Celsentri®), a CCR5-receptor antagonist, became available for treatment of patients infected with HIV-1.. Improvement of endothelial function may be a potential beneficial side effect of treatment with maraviroc, due to the potential reduction of immune activation and chronic inflammation as a result of blocking the CCR5-coreceptor. Moreover, treatment intensification of HAART with maraviroc in patients with suppressed plasma HIV_RNA may decrease plasma HIVRNA below the cut-off of 50 copies/ml as well.. The investigators hypothesize that maraviroc intensification therapy in patients on an abacavir-containing ...
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. Leung et al. (1989) demonstrated that culture media conditioned by human embryonic kidney cells expressing either bovine or human VEGF cDNA promoted proliferation of capillary endothelial cells. VEGF, a homodimeric glycoprotein of relative molecular mass 45,000, is the only mitogen that specifically acts on endothelial cells. It may be a major regulator of tumor angiogenesis in vivo. Millauer et al. (1994) observed in mouse that its expression was upregulated by hypoxia and that its cell surface receptor, Flk1 (KDR; 191306), is exclusively expressed in endothelial cells. 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. VEGF and ...
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. Leung et al. (1989) demonstrated that culture media conditioned by human embryonic kidney cells expressing either bovine or human VEGF cDNA promoted proliferation of capillary endothelial cells. VEGF, a homodimeric glycoprotein of relative molecular mass 45,000, is the only mitogen that specifically acts on endothelial cells. It may be a major regulator of tumor angiogenesis in vivo. Millauer et al. (1994) observed in mouse that its expression was upregulated by hypoxia and that its cell surface receptor, Flk1 (KDR; 191306), is exclusively expressed in endothelial cells. 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. VEGF and ...
The endothelium is an important regulator of the cardiovascular system by releasing nitric oxide, prostacyclin, endothelin-1, and other endothelium-derived constricting factors which are able to profoundly affect vascular tone and the function of circulating blood cells such as Format: Paperback.. Endothelium and Cardiovascular Diseases: Vascular Biology and Clinical Syndromes provides an in-depth examination of the role of endothelium and endothelial dysfunction in normal vascular function, and in a broad spectrum of clinical syndromes, from atherosclerosis, to cognitive disturbances and eclampsia.. The endothelium is a major participant in the pathophysiology of diseases, such as atherosclerosis, diabetes. Endothelium and Cardiovascular Diseases: Vascular Biology and Clinical Syndromes provides an in-depth examination of the role of endothelium and endothelial dysfunction in normal vascular function, and in a broad spectrum of clinical syndromes, from atherosclerosis, to cognitive disturbances ...
Mechanical forces have long been known to be potent regulators of vascular endothelial function.3 Endothelial cells have evolved sophisticated sensory and regulatory ability to maintain vascular homeostasis through adaptive remodeling.20 This study addresses the question of how endothelial cells respond to mechanical strain to control the growth of the underlying VSMCs. Previously, it was known that endothelial cells can regulate VSMC proliferation.21 In particular, heparin and endothelial cell HSPGs are potent inhibitors of VSMC proliferation and FGF-2 induced mitogenesis.13,22-24 This regulation is growth state dependent, with subconfluent cultures of endothelial cells stimulating VSMC growth and postconfluent cultures inhibiting VSMC growth.12,25-28 Similarly, perlecan and endothelial-derived HSPGs have been shown to be essential in inhibiting the neointimal response to vascular injury.14,29-31 Our study adds a new dimension to these results, demonstrating that the regulation of perlecan by ...
Results KLF2 upregulation profoundly ameliorated HSC phenotype (reduced α-smooth muscle actin, procollagen I and oxidative stress) partly via the activation of the nuclear factor (NF)-E2-related factor 2 (Nrf2). Coculture experiments showed that improvement in HSC phenotype paracrinally ameliorated liver sinusoidal endothelial cells probably through a vascular endothelial growth factor-mediated mechanism. No paracrine interactions between hepatocytes and HSC were observed. Cirrhotic rats treated with simvastatin or Ad-KLF2 showed hepatic upregulation in the KLF2-Nrf2 pathway, deactivation of HSC and prominent reduction in liver fibrosis. Hepatic KLF2 overexpression was associated with lower portal pressure (-15%) due to both attenuations in the increased portal blood flow and hepatic vascular resistance, together with a significant improvement in hepatic endothelial dysfunction. ...
4610 Tumor endothelial marker 7 (TEM-7) mRNA has been previously shown to be elevated in human colorectal cancer endothelium compared to normal adjacent colorectal endothelium (St. Croix et al., Science, 2000), and is a possible therapeutic target for antiangiogenic intervention in colorectal cancer.. We evaluated TEM-7 mRNA expression in human microvascular endothelial cells (HMVEC), human umbilical vein endothelial cells (HUVEC) and endothelial precursor cells (EPC). We found that TEM-7 was not expressed in either HMVEC or HUVEC but was present in EPC. We stimulated HMVEC, HUVEC and EPC with 100 nM of the phorbol ester PMA and found that TEM-7 mRNA was induced by PMA in EPC but not in HMVEC or HUVEC. Given that EPC are closer, at the molecular level, to tumor endothelium than they are to normal quiescent endothelium (Bagley et al., Cancer Research, 2003) and that PMA is a potent transcriptional activator of cancer-associated genes, the induction of TEM-7 by PMA in EPC suggests that TEM-7 may ...
Hematogenous metastasis requires the arrest and extravasation of blood-borne tumor cells, possibly involving direct adhesive interactions with vascular endothelium. Cytokine activation of cultured human endothelium increases adhesion of melanoma and carcinoma cell lines. An inducible 110-kD endothelial cell surface glycoprotein, designated INCAM-110, appears to mediate adhesion of melanoma cells. In addition, an inducible endothelial receptor for neutrophils, ELAM-1, supports the adhesion of a human colon carcinoma cell line. Thus, activation of vascular endothelium in vivo that results in increased expression of INCAM-110 and ELAM-1 may promote tumor cell adhesion and affect the incidence and distribution of metastases.. ...
The recruitment of leukocytes to sites of infection and their migration through the endothelium are critical to immune responses. Transendothelial migration is essential for leukocytes to respond to foreign microorganisms, but if uncontrolled, can cause autoimmune diseases such as inflammatory bowel disease and rheumatoid arthritis. In order to evaluate the transmigration of leukocytes, we have developed a kinetic, label-free in vitro assay to automatically acquire and analyze transendothelial migration, with the added ability to monitor monolayer integrity.. Using primary T cells and Human Umbilical Vein Endothelial cells (HUVEC), we evaluated the ability of this novel assay to quantify leukocyte transmigration in the absence of cell labeling. Briefly, endothelial cells were grown to confluence on a physiological surface. Leukocytes were added to the monolayer, and the upper chamber was placed into a reservoir plate containing chemoattractant. Live cell images were captured at regular ...
The ability of lysoPC, either independently or as a component of oxidized LDL, to inhibit endothelial-dependent vasorelaxation is well established (Cowan and Steffen, 1995; Freeman et al., 1996). The effect of lysoPC to impair endothelium-dependent relaxation is generalized to a variety of endothelium-dependent vasodilators, including acetylcholine (Kugiyama et al., 1990), 5-hyroxytryptamine (Cox and Cohen, 1996a), thrombin (Murohara et al., 1994) and calcium ionophore A23187 (Mangin et al., 1993). However, the cellular pathways affected by lysoPC that ultimately result in endothelial vasomotor dysfunction remain unclear. LysoPC was recently documented to stimulate PLD activity in cultured human endothelial cells (Cox and Cohen, 1996c), although the role of this effect in the vasomotor actions of lysoPC was not addressed. The present study has demonstrated the ability of lysoPC to stimulate vascular PLD activity in isolated blood vessels and has documented a close association between the ability ...
TY - JOUR. T1 - Endothelial cells regulate cardiac contractility. AU - Ramaciotti, Claudio. AU - Sharkey, Angela. AU - McClellan, George. AU - Winegrad, Saul. PY - 1992. Y1 - 1992. N2 - Endothelial cells lining the lumen of blood vessels contain the receptors for many substances that alter the contractile tone of smooth muscle in the walls of the blood vessels. In response to their interaction with the signal substances, the endothelial cells release vasoactive factors that modify the contractile state of the vascular smooth muscle. This study was conducted to determine if endothelial cells can also modulate the contraction of cardiac muscle cells and contribute to the physiological regulation of the heart. The venous effluent from the coronary circulation of an isolated perfused working heart was reoxygenated and used to superfuse a trabecula isolated from the right ventricle of another heart. The peak tension and the duration of the contraction of the trabecula were reversibly altered by the ...
Objective: Peroxisome proliferator-activated receptor γ (PPARγ) agonists reduce blood pressure (BP) and vascular injury in hypertensive rodents and humans. Pparγ inactivation in vascular smooth muscle cells (VSMC)using a tamoxifen inducible Cre-Lox system enhanced angiotensin II-induced vascular injury. Transgenic mice overexpressing endothelin (ET)-1selectively in the endothelium (eET-1) exhibit endothelial dysfunction, increased oxidative stress and inflammation. We hypothesized that inactivation of Pparγ in VSMC(smPparγ-/-)will exaggerate ET-1-induced vascular damage.. Methods and Results: Elevenweek-old male control, eET-1, smPparγ-/-and eET-1/smPparγ-/- mice weretreated with tamoxifen (1 mg/kg/day, s.c.) for 5 days and sacrificed 4 weeks later. Systolic BP was higher in eET-1compared to control (123±5 vs 109±2 mmHg,P,0.05)and unaffected by Pparγ inactivation.Mesenteric artery (MA) vasodilatory responses to acetylcholine were impaired only in smPparγ-/- (P,0.05) compared to ...
Inflammation and shear stress can upregulate expression of cellular adhesion molecules in endothelial cells (EC). The modified EC surface becomes a mediating interface between the circulating blood elements and the endothelium, and grants opportunity for immunotherapy. In photodynamic therapy (PDT), immunotargeting might overcome the lack of selectivity of currently used sensitizers. In this study, we hypothesized that differential ICAM-1 expression modulates the effects of a drug targeted to surface ICAM-1. A novel porphycene-anti-ICAM-1 conjugate was synthesized and applied to treat endothelial cells from macro and microvasculature. Results show that the conjugate induces phototoxicity in inflamed, but not in healthy, microvascular EC. Conversely, macrovascular EC exhibited phototoxicity regardless of their state. These findings have two major implications; the relevance of ICAM-1 as a modulator of drug effects in microvasculature, and the potential of the porphycene bioconjugate as a ...
This paper addresses the hypothesis that the expression of members of the NDST enzyme family can vary between different cell types and following stimulation by pro-inflammatory cytokines. The immortalized human microvascular endothelial cell line HMEC-1 was used to model the effect of cytokine-mediated regulation of NDST expression on the abundance of sulphated domains within HS on the surface of the vascular endothelium. This was followed by an examination of changes in the potential of these cells to bind exogenous RANTES at their apical surface and subsequent analysis of changes in the biological activity of this chemokine. The HMEC-1 cell line was chosen for this work as it provides a reproducible system which has previously been validated to model aspects of the immunobiology of microvascular endothelium including the uniform response to pro-inflammatory cytokines (Goebeler et al., 1997) and the presentation of antigens to specific T cells (Bosse et al., 1993). In addition, HMEC-1 cells are ...
A stable, in vitro cardiac endothelial cell line could provide high cell numbers as needed for many epigenetic analyses and facilitate the understanding of molecular mechanisms involved in endothelial cell biology. To test their suitability for transcriptomic or epigenetic studies, we compared the transcriptome of cultured immortalized mouse cardiac endothelial cells (MCEC) to primary cardiac endothelial cells (pEC). However, in MCEC we found a broad downregulation of genes that are highly expressed in pEC, including well-described markers of endothelial cell differentiation. Accordingly, systematic analysis revealed a downregulation of genes associated with typical endothelial cell functions in MCEC, while genes related to mitotic cell cycle were upregulated when compared to pEC. In conclusion, the findings from this study suggest that primary cardiac endothelial cells should preferably be used for genome-wide transcriptome or epigenome studies. The suitability of in vitro cell lines for ...
Aim: Evaluation of eNOS mRNA level in the endothelium of human coronary arteries upon opioids treatment (mediators of ischaemic preconditioning) and after incubation with proinflammatory cytokines (stress stimuli). Methods: Different concentrations of β-endorphin, endomorphin-1 and endomorphin-2 (alone or in combination with the opioid receptor blocker naloxone) as well as different concentrations of cytokines alone (IL-1β, TNF-α) or in combination were applied to in vitro cultured human coronary artery endothelial cells (HCAEC). After 24 hrs incubation, the cells were harvested, mRNA extracted and relative quantification of eNOS mRNA was conducted using real-time PCR. ...
Purpose - To study the effect of eggplant on endothelium-dependent relaxation, and plasma lipids in hypercholesterolemic rabbits, and to assess influence of this plant on the malondialdehyde (MDA) content of LDL particles and the arterial wall. Methods - Thirteen male rabbits were randomly assigned to control (C), hypercholesterolemic (H) and egg plant (E) treated groups (n=10 each). The H and Erabbits were fed a diet supplemented with cholesterol (0.5%) and coconut oil (10%) for 4 weeks. In addition, group E received 10mL of the fruit juice/day during the last 2 weeks. The animals were killed and the aorta removed to measure MDA content and the endothelium dependent relaxation responses. Total plasma cholesterol VLDL, LDL, HDL and triglyceride levels were determined using commercial kits. MDA was quantified in native and oxidized LDL and in the arterial wall. Results - After 4 weeks, the E group rabbits had a significantly lower weight, plasma cholesterol, LDL, triglyceride and aortic ...
The endothelium is the simple squamous epithelium that lines the innermost layer of the cardiovascular and lymphatic vessels and is continuous with the endocardial lining of the heart. Endothelial cells are active participants in a variety of vessel-related activities, including mechanical influences on blood flow, regulation of the transport of macromolecules and blood components from the interstitium to the lumen of the vessel, secretion of chemical mediators that influence the contractile state of the overlying smooth muscle, and contribution to capillary permeability. In addition, their smooth luminal surface facilitates efficient blood flow by reducing surface friction. The vascular endothelium is divided into arterial and venous endothelia, with additional differences between larger and smaller vessels.. The fenestrated endothelium, present in organs, such as the kidney and liver, that reabsorb water and small molecules or hormones, is characterized by the presence of circular windows in ...
In the past two decades, normal endothelial function has been identified as integral to vascular health. The endothelium produces numerous vasodilator and vasoconstrictor compounds that regulate vascular tone; the vasodilator, nitric oxide (NO), has additional antiatherogenic properties, is probably …
Emerging evidence indicates that brain microvascular endothelial cells play a critical role in brain development, maturation, and homeostasis. Acute or chronic insults, including oxidative stress, oxy
In the past two decades, normal endothelial function has been identified as integral to vascular health. The endothelium produces numerous vasodilator and vasoconstrictor compounds that regulate vascu
Mouse monoclonal antibody raised against Rat Endothelial Cell Antigen 1. Native purified from peripheral and mesenteric lymph nodes preparation. (MAB5196) - Products - Abnova
PeproTech offers three separate endothelial cell culture media formulations developed for the in vitro cultivation of: endothelial progenitor
Our data show that F-actin-anchored focal adhesions distinguish endothelial phenotypes of human arteries from veins. We conclude that the biomechanical properties of the vascular extracellular matrix determine this endothelial characteristic.
Supplementary MaterialsS1 Fig: COL6 does not enhance lung epithelial cell proliferation. pone.0209095.s004.docx (17K) GUID:?95A94D62-D70D-4D93-9A88-360DB426C86A S2 Text: Methods: buy BMS-354825 Human being lung fibroblast culture. (DOCX) pone.0209095.s005.docx (17K) GUID:?EF3D80B0-1A99-4F45-B95B-40D29CA9082E S1 Appendix: Minimal underlying dataset. (ZIP) (14K) GUID:?D1BC5B89-D8C4-4638-9E81-975B89B3496B Data Availability StatementAll relevant data are within the paper and its Supporting Information documents. Abstract Basement membrane (BM) … [Read more…]. ...
Summary. Endothelium was »discovered« as a separate organ in the last decades of the previous century. For a long time endothelial cells were considered as a very passive monolayer of cells just covering the inner part of vascular walls. The role of these cells was thought to be only a mechanical barrier between circulating blood and vascular structures. Nowadays, after a series of biochemical and experimental studies, one can name endothelium as an organ, covering approximately 700 sqaure meters, weighing about 1.5 kilos in an average male with weight of 70 kg. Not only its quantity, but also its function is amazing. The most prominent and first well studied function of endothelial cells is vasodilatation and vasoconstriction. Normal cells, which are intact and in function produce regularly one of the most important protecting agent in circulation: NO. Normal endothelial cells produce NO as a result of higher blood pressure or growing demand for oxygen. It is produced from aminoacid ...
We use cookies to ensure that we give you the best experience on our website. If you click Continue well assume that you are happy to receive all cookies and you wont see this message again. Click Find out more for information on how to change your cookie settings ...
Sigma-Aldrich offers abstracts and full-text articles by [Keiichi Torimoto, Yosuke Okada, Hiroko Mori, Takashi Otsuka, Mayuko Kawaguchi, Megumi Matsuda, Fumi Kuno, Kei Sugai, Satomi Sonoda, Maiko Hajime, Kenichi Tanaka, Tadashi Arao, Yoshiya Tanaka].
The endothelium is a thin mono-cellular layer which covers the inner surface of the blood vessels, separating the circulating blood from the tissues and also has the responsibility for uninterrupted maintenance of circulation to all the vital tissues. Endothelium is a very active organ, it works as a receptor-effector organ and responds to each physical or chemical stimulus with the release of the appropriate substance with which it may maintain vasomotor balance and vascular-tissue homeostasis. It has the property of producing, independently, both agonistic and antagonistic substances that help to keep homeostasis and its function is not only autocrine, but also paracrine and endocrine. In this way it modulates the vascular smooth muscle cells producing relaxation or contraction, and therefore vasodilatation or vasoconstriction.. The vascular endothelium is vulnerable to maximum wear and tear due to its positioning and requires prompt regeneration of the cells. Whenever the imbalance between ...
Its been eight years since I first put together research on MS as a disease connected to blood flow and the vascular system. What I saw in Jeffs blood results when he was diagnosed during his first severe flare---hypercoagulation, high c reactive protein, high inflammatory markers---looked to me like a vascular reaction caused by endothelial dysfunction. I sent the research I compiled to university researchers, and created a nutrition and lifestyle program for Jeff, to address this issue. My hope was that he could find stability in his disease process, by reducing the impact of vascular endothelial dysfunction. I saw that cardiovascular researchers, like Dr. John Cooke, were having great success with their heart patients, and that encouraged me! And sure enough, after three months on the Endothelial Health Program, Jeffs serum markers of endothelial dysfunction were lowered, and his MS stayed in remission ...
The endothelium is the single-cell-thick interior lining of all blood vessels in the body. Dilation of blood vessels is enabled by endothelial cells, which release vasodilators like nitric oxide (NO) in response to increased blood flow. The percentage difference in diameter between fully dilated and resting blood vessels is known as flow-mediated dilation (FMD). Healthier vessels release more NO, leading to a higher FMD and a lower risk of CVD and atherosclerosis. The AngioDefender™ system measures these sensitive changes, then calculates and converts them into an FMD score. The process behind FMD is illustrated below.. ...
The endothelium is the single-cell-thick interior lining of all blood vessels in the body. Dilation of blood vessels is enabled by endothelial cells, which release vasodilators like nitric oxide (NO) in response to increased blood flow. The percentage difference in diameter between fully dilated and resting blood vessels is known as flow-mediated dilation (FMD). Healthier vessels release more NO, leading to a higher FMD and a lower risk of CVD and atherosclerosis. The AngioDefender™ system measures these sensitive changes, then calculates and converts them into an FMD score. The process behind FMD is illustrated below.. ...
Specific Aims Transforming growth factor (TGF-?) superfamily signaling in endothelial cells regulates essential components of angiogenesis and vascular morphoge...
In a study that could point to novel therapies to prevent cancer spread, or metastasis, researchers have targeted a sugar that supports blood vessel growth in the tumor.
Endothelial Dysfunction - Old Concepts and New Challenges. Edited by: Helena Lenasi. ISBN 978-1-78984-253-1, eISBN 978-1-78984-254-8, PDF ISBN 978-1-83881-339-0, Published 2018-10-24
Es are in constant physical contact with the EC surface. Additionally, in the brains of both mice and human with CM, leukocytes (monocytes and T cells) become
Click on a genes description to view its network relationships with genes known to be involved in regulation of blood vessel endothelial cell migration ...
Bussolino F, Valdembri D, Caccavari F, Serini G (2006). "Semaphoring vascular morphogenesis". Endothelium. 13 (2): 81-91. doi: ... vascular remodeling, and growth cone collapse. Both upregulation and downregulation of Plexin A4 has been observed following ...
... but also to the ability of the vascular endothelium to aid in the regulation of vascular tone, prevention of vascular rigidity ... Vascular endotheliumEdit. Endothelium is a thin layer of simple squamous epithelial cells that line the interior of both blood ... The endothelium that lines blood vessels is known as vascular endothelium, which is subject to and must withstand the forces of ... Depolarization in vascular endothelium is essential not only to the structural integrity of endothelial cells, ...
Atanu Basu, Umesh C. Chaturvedi (June 2008). "Vascular endothelium: the battlefield of dengue viruses". FEMS Immunology and ...
Minami T, Sugiyama A, Wu SQ, Abid R, Kodama T, Aird WC (January 2004). "Thrombin and phenotypic modulation of the endothelium ... migration and proliferation of vascular smooth muscle cells, apoptosis and angiogenesis. Thrombin is implicated in the ... ". Arteriosclerosis, Thrombosis, and Vascular Biology. 24 (1): 41-53. doi:10.1161/01.ATV.0000099880.09014.7D. PMID 14551154. De ...
Gimbrone MA Jr, García-Cardeña G (2013). "Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis". ... Aortic vascular smooth muscle cells failed to organize into a normal tunica media, and pericytes were low in number. These KLF2 ... KLF2 expression is induced by fluid laminar flow shear stress, as is caused by blood flow in normal endothelium. This activates ... It is expressed as early as embryonic day 9.5 in the endothelium. KLF2 has a particularly interesting expression profile in ...
Yao Y, Jumabay M, Ly A, Radparvar M, Cubberly MR, Boström KI (2013). "A role for the endothelium in vascular calcification". ... The protein acts as an inhibitor of vascular mineralization and plays a role in bone organization. MGP is found in a number of ...
NO produced by eNOS in the vascular endothelium plays crucial roles in regulating vascular tone, cellular proliferation, ... In the vascular endothelium, NO is synthesized by eNOS from L-arginine and molecular oxygen, which binds to the heme group of ... eNOS is primarily responsible for the generation of NO in the vascular endothelium, a monolayer of flat cells lining the ... Moreover, NO affects leukocyte adhesion to the vascular endothelium by inhibiting the nuclear factor kappa B (NF-κB), which ...
Vascular lesions[edit]. These result from injury to the vascular endothelium. Causes:. Venoocclusive disease: Chemotherapeutic ...
... including vascular SMCs and in platelets. Lower levels are present in vascular endothelium and cardiomyocytes. The enzyme is ... but not in cardiac and vascular myocytes. Specifically, in smooth muscle tissue, PKG promotes the opening of calcium-activated ...
Monahan-Earley, R.; Dvorak, A. M.; Aird, W. C. (2013). "Evolutionary origins of the blood vascular system and endothelium". ... Muscular tissue of heart Major systems of the human body Amato Lusitano Vascular resistance - Vascular resistance is the ... The blood vascular system first appeared probably in an ancestor of the triploblasts over 600 million years ago, overcoming the ... Vascular surgeons focus on other parts of the circulatory system. The essential components of the human cardiovascular system ...
1970) Circulating endothelium as an indicator of vascular injury. Thromb Diath Haemorrh. 40: 163-168 Mutin, M., Canavy, I., ... 48: 1538-1547 Bouvier, C.A., Gaynor, E., Clintron, J.R. et al (1970) Circulating endothelium as an indicator of vascular injury ... are cells derived from the bone marrow which differentiate into endothelial cells to help support the vascular endothelium and ... Biomarker of vascular disease. Thromb Haemost. 93: 228-235. George, F., Brisson, C., Poncelet, P., Laurent, J.C., Massot, O., ...
Ribatti D (2008). "Napoleone Ferrara and the saga of vascular endothelial growth factor". Endothelium. 15 (1): 1-8. doi:10.1080 ... 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, Domenico (2008). "Napoleone Ferrara and the saga of vascular endothelial growth factor". Endothelium: Journal of ... vascular endothelial growth factor' in 1989, while working at Genentech. He is credited with developing a whole new class of ...
February 27, 2004 F.D.A. Approves Cancer Drug From Genentech Ribatti D (2008). "Napoleone Ferrara and the saga of vascular ... endothelial growth factor". Endothelium. 15 (1): 1-8. doi:10.1080/10623320802092377. PMID 18568940. "FDA Approval for ... In addition to directing the Children's Hospital Boston Surgical Research Laboratories, which grew to become the Vascular ... Biology Program, for nearly four decades, he was the Scientific Director of the hospital's Vascular Anomalies Center. In 1971, ...
His scientific work concerns vascular biology and pharmacology of endothelium. His research focuses on the mechanisms of ...
AVPR2 is also expressed outside the kidney in vascular endothelium. Stimulation causes the release of von Willebrand factor and ...
Shibuya N, Mikami Y, Kimura Y, Nagahara N, Kimura H (November 2009). "Vascular endothelium expresses 3-mercaptopyruvate ...
2005). "CLEVER-1 mediates lymphocyte transmigration through vascular and lymphatic endothelium". Blood. 104 (13): 3849-57. doi: ... 2005). "Stabilin-1 and stabilin-2 are both directed into the early endocytic pathway in hepatic sinusoidal endothelium via ... 2003). "The same endothelial receptor controls lymphocyte traffic both in vascular and lymphatic vessels". Eur. J. Immunol. 33 ...
Some unknown factors cause vascular damage in the endothelium, causing hypertension. If severe, it progresses to eclampsia, ...
IL-1 activates resident lymphocytes and vascular endothelia. *TNFα increases vascular permeability and activates vascular ... interact and effectively pull the cell through the endothelium. Once through the endothelium, the leukocyte must penetrate the ... and other vascular ligands. It has been hypothesized that low forces decrease L-selectin-PSGL-1 off-rates (catch bonds), ... endothelia. *CXCL8 (IL-8) forms a chemotactic gradient that directs leukocytes towards site of tissue injury/infection (CCL2 ...
In Vascular endothelium in health and disease (Vol. 242, pp. 3-5). New York City, New York: Plenum Press. Capillaries. (n.d.). ... In capillary endothelium, plasma communicates with the interstitial fluid through the intercellular cleft. Blood plasma without ... Most notably, intercellular clefts are often found between epithelial cells and the endothelium of blood vessels and lymphatic ... The organization of the endocardial endothelium and the intercellular cleft help to establish the blood-heart barrier by ...
MS has an important vascular component. Postmortem studies of the BBB, especially the vascular endothelium, show immunological ... Endothelium: Other theories point to a possible primary endothelial dysfunction. The importance of vascular misbehaviour in MS ... Possibly vascular problems may be an aggravating factor, like many others in MS. Indeed, the research, by demonstrating ... It is reported that a number of studies have provided evidence of vascular occlusion in MS, which suggest the possibility of a ...
"Migration of human hematopoietic progenitor cells across bone marrow endothelium is regulated by vascular endothelial cadherin ... "Real-time imaging of vascular endothelial-cadherin during leukocyte transmigration across endothelium". J. Immunol. 167 (4): ... "Functional properties of human vascular endothelial cadherin (7B4/cadherin-5), an endothelium-specific cadherin". Arterioscler ... "Vascular endothelial growth factor induces SHC association with vascular endothelial cadherin: a potential feedback mechanism ...
Endothelium dysfunction is a prototypical characteristic of vascular disease, which is common in patients with autoimmune ... Tal1 gene is specifically found in the vascular endothelium and developing brain.[5] This gene encodes the basic helix-loop- ... Lymphatic-specific vascular endothelial growth factors VEGF-C and VEGF-D function as ligands for the vascular endothelial ... The vascular system is made up of two parts: 1) Blood vasculature 2) Lymphatic vessels Both parts consist of ECs that show ...
Chiu, Jeng-Jiann; Chien, Shu (2011-01-01). "Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and ...
"Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives". Physiological Reviews. ...
Necrosis of the endothelium is microscopically evident. The mechanism of transplacental infection has been investigated by ... This seems to preclude further development of the vascular network of the conceptus. Preparation for cellular mitosis (i.e., ... One of the most striking features of viral distribution is the extensive involvement of endothelium. ... and it is probable that microscopic lesions of necrosis and vascular damage, subsequently described for fetuses, also develop ...
2001). "Regeneration of ischemic cardiac muscle and vascular endothelium by adult stem cells". J Clin Invest. 107 (11): 1395- ... 2009). "Hepatocyte growth factor or vascular endothelial growth factor gene transfer maximizes mesenchymal stem cell-based ... interest in attempting to develop such products to treat conditions including Crohn's disease and a variety of vascular ...
"Leukocyte adhesion to vascular endothelium induces E-selectin linkage to the actin cytoskeleton". The Journal of Cell Biology. ...
The functional capacity of selectin is limited to leukocyte collaborations with vascular endothelium. There are three types of ... P-selectin deals with platelets and endothelium and E-selectin deals only with endothelium. They have extracellular regions ... Tedder TF, Steeber DA, Chen A, Engel P (July 1995). "The selectins: vascular adhesion molecules". FASEB Journal. 9 (10): 866-73 ...
Mice engineered to specifically have vascular endothelium cells deficient in β-catenin showed disrupted adhesion between ... 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 ... vascular endothelial cells. Mice lacking plakoglobin have cell adhesion defects in many tissues, although β-catenin substitutes ...
It has been shown that vasodilatation to substance P is dependent on the NK1 receptor located on the endothelium. In contrast ... "Substance P enhances cytokine-induced vascular cell adhesion molecule-1 (VCAM-1) expression on cultured rheumatoid fibroblast- ... "In vivo measurement of endothelium-dependent vasodilation with substance P in man". Herz. 17 (5): 284-90. PMID 1282120.. ... endothelia of capillaries and lymphatics, fibroblasts, stem cells, white blood cells) in many tissues and organs. SP amplifies ...
The rate at which fluid is filtered across vascular endothelium (transendothelial filtration) is determined by the sum of two ...
It has been hypothesized that vascular endothelial growth factor may cause the vascular permeability at the root of HACE.[16] ... The leaking may be caused by increased pressure, or it may be caused by inflammation that makes the endothelium vulnerable to ... Hypoxia increases extracellular fluid, which passes through the vasogenic endothelium in the brain. ... This in turn can increase vascular permeability and causes edema. This may combine with low levels of cytokines to cause HACE.[ ...
t-PA is released into the blood very slowly by the damaged endothelium of the blood vessels, such that, after several days ( ... and fibrin degradation products have some vascular permeability inducing effects. ...
The damage to the endothelium and the alveolar epithelium results in the creation of an open interface between the lung and the ... such as the effects of inflammatory mediators on airway and vascular smooth muscle tone. As a rule of thumb, all these models ... the endothelium and the basement membrane of the alveolus. In the acute phase of ALI, there is increased permeability of this ... is affected by increases in the dispersion of both alveolar ventilation and cardiac output because bronchial and vascular ...
The canal is essentially an endothelium-lined tube, resembling that of a lymphatic vessel. On the inside of the canal, nearest ... "Schlemm's canal is a unique vessel with a combination of blood vascular and lymphatic phenotypes that forms by a novel ... Ramos RF, Hoying JB, Witte MH, Daniel Stamer W. (2007). "Schlemm's canal endothelia, lymphatic, or blood vasculature?". J ... discovered that Schlemm's canal displays several features of lymphatic endothelium, including the expression of PROX1, VEGFR3, ...
High blood pressure in the long term can damage the endothelium, commonly known as the blood vessel lining. This leads to a ... Microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular ... Kidney disease with this etiology can potentially be reversed following vascular intervention. ...
The endothelium is a layer of cells that line the interior surface of blood vessels. Endothelial dysfunction is implicated in ... many aspects of vascular diseases. The researchers noted that the effect of vitamin C supplementation appeared to be dependent ...
The endothelium maintains vascular homeostasis through the release of active vasodilators. Although Nitric Oxide (NO) is ... Endothelium-derived hyperpolarizing factor. In blood vessels Endothelium-Derived Hyperpolarizing Factor or EDHF is proposed to ... However, once the involvement of a certain endothelium-derived vasodilator for a given vascular bed is confirmed, it is ... Luksha L, Agewall S, Kublickiene K (February 2009). "Endothelium-derived hyperpolarizing factor in vascular physiology and ...
It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also ... Bradykinin dilates blood vessels via the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor ... Bradykinin is a potent endothelium-dependent vasodilator, leading to a drop in blood pressure. ...
"Dipyridamole for preventing stroke and other vascular events in patients with vascular disease". Julius Center for General ... Zat ini tampaknya bekerja pada pelapis pembuluh darah atau endothelium. Sayangnya, setelah percobaan yang pertama berhasil, ... Interdisciplinary Council on Peripheral Vascular Disease.; Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E ... noninvasive vascular imaging, dan saat memungkinkan dan relevan, angiografi. Dari diagnosa tersebut subtipe infarcts of ...
Azzopardi G.; Petkov N. (2011). Detection of retinal vascular bifurcations by trainable V4-like filters, in Computer Analysis ... The mapping of vascular bifurcations is one of the basic steps in biometric identification.[45] Results of such analyses of ... "Retinal fundus images - Ground truth of vascular bifurcations and crossovers". University of Groningen. Retrieved 20 April 2018 ... In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it ...
... is an uncommon vascular condition characterised by multiple, randomly distributed, blood-filled cavities ... the blood-filled spaces are lined with endothelium and are associated with aneurysmal dilatation of the central vein; in the ...
Kidney disease with this etiology can potentially be reversed following vascular intervention. In benign nephrosclerosis, the ... High blood pressure in the long term can damage the endothelium, commonly known as the blood vessel lining. This leads to a ... is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. ...
... it is synthesized and released into the bloodstream by the vascular, glomerular, and tubular endothelium, and the sinusoidal ...
On vascular smooth muscle cells if not otherwise specified Transduction (↑ = increases. ↓ = decreases)[4]. ... Arginine vasopressin receptor on endothelium. Endothelin production[5]. *Products of platelet activation[5] ... The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca2+ ions) within vascular ... When blood vessels constrict, the flow of blood is restricted or decreased, thus retaining body heat or increasing vascular ...
... except in the central nervous system and non-vascular tissues) which serve to drain and process extracellular fluid. Upon ...
The word vascular, meaning relating to the blood vessels, is derived from the Latin vas, meaning vessel. A few structures (such ... Permeability of the endothelium is pivotal in the release of nutrients to the tissue. It is also increased in inflammation in ... Main article: Vascular disease. Blood vessels play a huge role in virtually every medical condition. Cancer, for example, ... Main article: Vascular resistance. The blood pressure in blood vessels is traditionally expressed in millimetres of mercury (1 ...
Endothelial cells are involved in many aspects of vascular biology, including: *Barrier function - the endothelium acts as a ... "Endothelium" at Dorland's Medical Dictionary *^ Eskin, S.G.; Ives, C.L.; McIntire, L.V.; Navarro, L.T. "Response of cultured ... "Arteriosclerosis, Thrombosis, and Vascular Biology. 36: 1090-100. doi:10.1161/ATVBAHA.115.306964. PMC 4882253. PMID 27127201.. ... Endothelium refers to cells that line the interior surface of blood vessels and lymphatic vessels,[1] forming an interface ...
"Metformin is not just an antihyperglycaemic drug but also has protective effects on the vascular endothelium". Acta ...
Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization ...
Another main function of the glycocalyx within the vascular endothelium is that it shields the vascular walls from direct ... In vascular endothelial tissue[edit]. The glycocalyx is located on the apical surface of vascular endothelial cells which line ... "Arteriosclerosis, Thrombosis, and Vascular Biology. 31 (8): 1908-1915. doi:10.1161/ATVBAHA.111.225268. PMC 3141106. Retrieved ... Whatever the stimulus is, however, shedding of the glycocalyx leads to a drastic[clarification needed] increase in vascular ...
It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural ... NO produced by eNOS has been shown to be a vasodilator identical to the endothelium-derived relaxing factor produced in ... In mammals, the endothelial isoform is the primary signal generator in the control of vascular tone, insulin secretion, and ... Specifically, NO has been shown to play an important negative feedback regulatory role on NOS3, and therefore vascular ...
Uvea/vascular tunic (middle). Choroid. *Capillary lamina of choroid. *Bruch's membrane. *Sattler's layer ...
Angiology (vascular)Edit. Intravascular ultrasound image of a coronary artery (left), with color-coding on the right, ... to visualize the endothelium (inner wall) of blood vessels in living individuals.[1] ... automatic classification of the vascular signature into a unique parameter, this last coded in one of the four following colors ... In angiology or vascular medicine, duplex ultrasound (B Mode imaging combined with Doppler flow measurement) is used to ...
Overcoming acute vascular rejection[edit]. Due to its complexity, the use of immunosuppressive drugs along with a wide array of ... The endothelium activation is considered type II since gene induction and protein synthesis are involved. The binding of XNAs ... Acute vascular rejection[edit]. Also known as delayed xenoactive rejection, this type of rejection occurs in discordant ... Acute vascular rejection requires de novo protein synthesis and is driven by interactions between the graft endothelial cells ...
Thiamine (vitamin B(1)) improves endothelium-dependent vasodilatation in the presence of hyperglycemia. Annals of Vascular ... High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia 2007 Aug ... Regulation of intracellular glucose and polyol pathway by thiamine and benfotiamine in vascular cells cultured in high glucose ... Regulation of intracellular glucose and polyol pathway by thiamine and benfotiamine in vascular cells cultured in high glucose ...
... on the vascular endothelium. The enzyme that carries out the carboxylation of glutamic acid is gamma-glutamyl carboxylase. The ... Several studies have also implicated warfarin use in valvular and vascular calcification. No specific treatment is available, ... "Association of warfarin use with valvular and vascular calcification: a review". Clinical Cardiology. 34 (2): 74-81. doi: ...
In view of the participation of vascular endothelial cells (EC) in a wide range of normal and pathological conditions, ... Antigenic Heterogeneity of Vascular Endothelium. In: Catravas J.D., Callow A.D., Gillis C.N., Ryan U.S. (eds) Vascular ... In view of the participation of vascular endothelial cells (EC) in a wide range of normal and pathological conditions, ... Endothelium. NATO ASI Series (Series A: Life Sciences), vol 208. Springer, Boston, MA. * DOI ...
Potassium softens vascular endothelium and increases nitric oxide release. H. Oberleithner, C. Callies, K. Kusche-Vihrog, H. ... Potassium softens vascular endothelium and increases nitric oxide release. H. Oberleithner, C. Callies, K. Kusche-Vihrog, H. ... Potassium softens vascular endothelium and increases nitric oxide release. H. Oberleithner, C. Callies, K. Kusche-Vihrog, H. ... Potassium softens vascular endothelium and increases nitric oxide release Message Subject (Your Name) has sent you a message ...
To determine whether the vascular endothelium contributes osteoprogenitor cells to vascular calcification. ... A role for the endothelium in vascular calcification.. Yao Y1, Jumabay M, Ly A, Radparvar M, Cubberly MR, Boström KI. ... However, it is not clear whether the vascular endothelium has a role in contributing osteoprogenitor cells to the calcific ... Our data suggest that the endothelium is a source of osteoprogenitor cells in vascular calcification that occurs in disorders ...
Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:2301-2310, originally published October 19, 2017 ... Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:2136-2146, originally published October 5, 2017 ... Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:1860-1868, originally published August 3, 2017 ... Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:A543, originally published August 25, 2017 ...
VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration.. Hamilla SM1, Stroka ... VE-Cadherin-Independent Cancer Cell Incorporation into the Vascular Endothelium Precedes Transmigration ... VE-Cadherin-Independent Cancer Cell Incorporation into the Vascular Endothelium Precedes Transmigration ... VE-Cadherin-Independent Cancer Cell Incorporation into the Vascular Endothelium Precedes Transmigration ...
Keywords: airway hyperresponsiveness; atopy; fibroblast growth factor; transforming growth factor-β; vascular endothelial ... Distinct association of genetic variations of vascular endothelial growth factor, transforming growth factor-β, and fibroblast ... whereas high levels of vascular endothelial growth factor (VEGF) enhanced airway sensitization to allergens and airway ...
Cancer cell migration through the endothelium and int … ... Cancer cell migration through the endothelium and into the ... VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration PLoS One. 2014 Oct 2;9( ... Here, we used a previously established in vitro model of the endothelium and live cell imaging, in order to observe cancer cell ... This process is well characterized for immune cells that routinely transmigrate through the endothelium to sites of infection, ...
... vascular cell adhesion molecule-1, and VEGF) were determined by the multiplex assay. After the single injection of both types ... affects the vascular infarction-related molecules (VIRMs). Nineteen eyes with DME were treated with 0.5 mg of intravitreal ... To determine whether an intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) in eyes with diabetic ... Expression of vascular infarction-related molecules after anti-vascular endothelium growth factor treatment for diabetic ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
Graft endothelium is indeed the first barrier between self and non-self that is encountered by host lymphocytes upon ... Graft endothelium is indeed the first barrier between self and non-self that is encountered by host lymphocytes upon ... the factors that foster graft endothelium functioning in spite of rejection, and how they could be therapeutically harnessed to ... This review of clinical and experimental studies aims at analyzing the interplay between graft endothelium and host immune ...
Age-related changes in P2-purinergic receptors on vascular smooth muscle and endothelium.. T Koga, Y Takata, K Kobayashi, K ... Age-related changes in P2-purinergic receptors on vascular smooth muscle and endothelium. ... Age-related changes in P2-purinergic receptors on vascular smooth muscle and endothelium. ... Age-related changes in P2-purinergic receptors on vascular smooth muscle and endothelium. ...
Culture of vascular endothelium. Prog Hemost Thromb 1976. 3:1-28. View this article via: PubMed Google Scholar ... Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages. Amir Kol ... Cytokines regulate vascular functions related to stability of the atherosclerotic plaque. J Cardiovasc Pharmacol 1995. 25(Suppl ... Libby, P, Li, H. Vascular cell adhesion molecule-1 and smooth muscle cell activation during atherogenesis. J Clin Invest 1993. ...
Tubular paramyxovirus-like structures in synovial vascular endothelium. Message subject: (Your Name) has forwarded a page to ...
Vascular endothelium responds to fluid shear stress gradients.. N DePaola, M A Gimbrone, P F Davies, C F Dewey ... In vitro investigations of the responses of vascular endothelium to fluid shear stress have typically been conducted under ... Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:1254-1257, originally published November 1, 1992 ... Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:1254-1257, originally published November 1, 1992 ...
Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium ... Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium ... Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium ... Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium ...
... and interacting chemical inputs to the vascular endothelium. The endothelium processes the entirety of the chemical composition ... The vascular endothelium is a continuous network of about 10 trillion cells (1) that controls virtually all cardiovascular ... Pressure-dependent regulation of Ca2+ signalling in the vascular endothelium. J. Physiol. 593, 5231-5253 (2015).. ... Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium ...
Non-invasive Imaging of Tissue-Engineered Vascular Endothelium with Iron Oxide Nanoparticles ... Non-invasive Imaging of Tissue-Engineered Vascular Endothelium with Iron Oxide Nanoparticles ... Non-invasive Imaging of Tissue-Engineered Vascular Endothelium with Iron Oxide Nanoparticles. ... Immobilization and Controlled Release of Vascular (VEGF) and Bone Growth Factors (BMP-2) on Bone Replacement Materials ...
Endothelial modulation was similar in both sets of arteries, suggesting that the endothelium does not mask an increased ... There was a positive correlation between blood pressure and vascular structure, suggesting that blood pressure is a major ... determinant of vascular structure. Only ACE inhibitor treatment normalised resistance vessel contractility and endothelium- ... Treatment also prevented the development of impaired endothelium-dependent relaxation. Treatment of SHRs with either an ACE ...
Leukocyte transmigration through the vascular endothelium is a key step in the immune response, and also in progression of the ... A novel in vitro model of the vascular endothelium was created. This model mimics physiological conditions more closely than ... These results indicate, for the first time, that the biophysical states of the endothelium and subendothelial matrix, which ... junctional protein organization in the endothelium, and signaling pathways. However, in recent years, many studies have ...
Psycho-Neuro-Immune-Endocrine System, Vascular Endothelium and Heart Failure. L. Lorente, M.-A. Aller, J. Arias ... Psycho-Neuro-Immune-Endocrine System, Vascular Endothelium and Heart Failure Message Subject (Your Name) has forwarded a page ...
This is a method to visualise leukocyte adhesion to the endothelium in harvested pressurised vessels. The technique enables ... Imaging Leukocyte Adhesion to the Vascular Endothelium at High Intraluminal Pressure. Danielle L. Michell1, Karen L. Andrews1, ... Michell, D. L., Andrews, K. L., Woollard, K. J., Chin-Dusting, J. P. Imaging Leukocyte Adhesion to the Vascular Endothelium at ... Methods employed in previous in vitro studies have demonstrated that acute increases in pressure on the endothelium can lead to ...
Fever-Range Hyperthermia Enhances L-Selectin-Dependent Adhesion of Lymphocytes to Vascular Endothelium. Wan-Chao Wang, Lorin M ... The effects of fever-range temperatures on lymphocyte adhesion to vascular endothelium was assessed in a Stamper-Woodruff ... Fever-Range Hyperthermia Enhances L-Selectin-Dependent Adhesion of Lymphocytes to Vascular Endothelium ... Fever-Range Hyperthermia Enhances L-Selectin-Dependent Adhesion of Lymphocytes to Vascular Endothelium ...
177 Pro-inflammatory signalling in vascular endothelium: a novel role for camkii in ageing? ... 177 Pro-inflammatory signalling in vascular endothelium: a novel role for camkii in ageing? ... This will establish involvement of CaMKIIδ in modulation of NF-kB signalling in a vascular endothelial cell line. Studies can ... Here we (i) characterise NF-kβ signalling in vascular endothelial cells and examine the potential for CaMKII modulation and (ii ...
Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of ... Gpr116 Receptor Regulates Distinctive Functions in Pneumocytes and Vascular Endothelium. Niaudet, Colin Uppsala University, ... Vascular BiologyDepartment of Immunology, Genetics and Pathology In the same journal. PLoS ONE On the subject. Immunology in ... Further analysis of this knockout model revealed cerebral vascular leakage, beginning at around 1.5 months of age. Additionally ...
The effects of a reduction in serum Hcy levels on the vascular endothelium in patients affected by PCOS have not been ... Effects of Metformin With or Without Supplementation With Folate on Homocysteine Levels and Vascular Endothelium of Women With ... Effects of Metformin With or Without Supplementation With Folate on Homocysteine Levels and Vascular Endothelium of Women With ... Effects of Metformin With or Without Supplementation With Folate on Homocysteine Levels and Vascular Endothelium of Women With ...
PGI2 and NO from endothelium) and by endothelium-independent mechanisms (Ca2+ influx control on smooth muscle cells). ... Therefore, these results indicate that Mokuboito and its constituents exert both vasodilating actions mediated by endothelium- ...
Vascular Endothelium: Responses to Injury has 2 available editions to buy at Alibris ... Vascular Endothelium: Responses to Injury by Allan D Callow (Editor), John D Catravas (Editor), Una S Ryan (Editor) starting at ... Vascular Endothelium: Responses to Injury. by Allan D Callow (Editor), John D Catravas (Editor), Una S Ryan (Editor) Write The ...
The vascular endothelium is versatile and multifunctional having, in addition to its role as a selective permeability barrier, ... A unifying system : does the vascular endothelium have a role to play in Multi-Organ Failure following radiation exposure ? ... investigators have increasingly recognized the importance of the endothelium as a central regulator of vascular and body ... many synthetic and metabolic properties including the modulation of vascular tone and blood flow, regulation of immune and ...
Vascular endothelium provides a selective barrier between the blood and tissues, participates in wound healing and angiogenesis ... IKK\(\beta\) -deleted endothelium manifests increased vascular permeability and reduced migration. Surprisingly, we find that ... IKK\(\beta\) Regulates Essential Functions of the Vascular Endothelium Through Kinase-Dependent and -Independent Pathways. ... IKK\(\beta\) regulates essential functions of the vascular endothelium through kinase-dependent and -independent pathways. ...
  • Abstract Since NO production is dependent on the availability of l -arginine, we examined whether l -arginine transport and NO synthesis are coregulated by vascular smooth muscle cells and endothelial cells cultured from the same vessel wall source. (
  • Abstract Endothelial cells release several compounds, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF), that mediate the vascular effects of vasoactive hormones. (
  • Blood flow, blood clotting, angiogenesis, vascular permeability, and vascular remodeling are each controlled by a large number of variable, noisy, and interacting chemical inputs to the vascular endothelium. (
  • The vascular endothelium is versatile and multifunctional having, in addition to its role as a selective permeability barrier, many synthetic and metabolic properties including the modulation of vascular tone and blood flow, regulation of immune and inflammatory responses, and regulation of coagulation, fibrinolysis, and thrombosis. (
  • IKK\(\beta\) -deleted endothelium manifests increased vascular permeability and reduced migration. (
  • PMN accumulation in the lung (myeloperoxidase assay), bronchoalveolar lavage (BAL) fluid, and lung vascular permeability (protein content in BAL fluid) were assessed 6 h later. (
  • The obtained results indicated that systemically administered CORM-3 attenuates PMN accumulation and vascular permeability in the septic lung. (
  • This study aimed to test the hypothesis that transforming growth factor (TGF)-β1 increases the paracellular permeability of vascular endothelial monolayers through tyrosine phosphorylation of VE-cadherin and claudin-5. (
  • Our results suggest that tyrosine phosphorylation of VE-cadherin and claudin-5 is involved in the increased paracellular permeability of central nervous system-derived vascular endothelium induced by TGF-β1. (
  • They maintain dynamic barrier properties responsive to multiple vascular permeability factors. (
  • Activation of Vascular Endothelial Growth Factor (VEGF) Receptor 2 Mediates Endothelial Permeability Caused by Cyclic Stretch. (
  • Role of Krev Interaction Trapped-1 in Prostacyclin-Induced Protection against Lung Vascular Permeability Induced by Excessive Mechanical Forces and Thrombin Receptor Activating Peptide 6. (
  • The vascular endothelium is a highly dynamic multifunctional organ that is critically involved in the regulation of vessel integrity, vascular growth and remodeling, tissue growth and metabolism, immune responses, cell adhesion, angiogenesis, hemostasis and vascular permeability [23]. (
  • Excessive or prolonged increases in permeability of the endothelium, as in cases of chronic inflammation, may lead to tissue swelling (edema). (
  • Ménage à trois: aldosterone, sodium and nitric oxide in vascular endothelium. (
  • Generally, VEGF plays an important role in physiological vascular angiogenesis and restoring homeostasis after ischemia-reperfusion conditions due to a cerebral infarction or a myocardial infarction. (
  • Vascular endothelium provides a selective barrier between the blood and tissues, participates in wound healing and angiogenesis, and regulates tissue recruitment of inflammatory cells. (
  • In this strategic position, they play a key role in a large number of important physiological processes, such as regulation of vascular tone and blood flow, fluid and solute exchange, haemostasis and coagulation, inflammatory responses and angiogenesis. (
  • Tissue damage disrupts the vascular endothelium, directly exposes blood enzymes to tissue factor, and activates the tissue repair mechanism that governs a predictable sequence of coagulation, inflammation, chemotaxis, mitosis, metabolism, immune activity and angiogenesis to enable tissue repair. (
  • Constriction and enlargement of the blood vessel, called vasoconstriction and vasodilation, and hence the control of blood pressure The endothelium is involved in the formation of new blood vessels, called angiogenesis. (
  • The general outline of angiogenesis is activating signals binding to surface receptors of vascular endothelial cells. (
  • Thank you for your interest in spreading the word on Arteriosclerosis, Thrombosis, and Vascular Biology. (
  • Your Name) thought you would like to see the Arteriosclerosis, Thrombosis, and Vascular Biology web site. (
  • Regulation of vascular tone during pregnancy: a novel role for the pregnane X receptor. (
  • The HIF-a hydroxylase system is a key player in the regulation of vascular remodeling. (
  • The vascular endothelium comprises the thin inner layer of cells lining arteries and veins, with an essential role in the regulation of blood vessel tone and cellular activity. (
  • Tare, M , Coleman, HA & Parkington, HC 2003, ' Regulation of vascular smooth muscle relaxation by the endothelium in health and in diabetes (with a focus on endothelium-derived hyperpolarizing factor) ', Neurophysiology , vol. 35, no. 3/4, pp. 256 - 261. (
  • These Nrp-plexin and semaphorin complexes initiate cascades that regulate diverse processes such as axon pruning and repulsion, dendritic attraction and branching, regulation of cell migration, vascular remodeling, and growth cone collapse. (
  • This process is well characterized for immune cells that routinely transmigrate through the endothelium to sites of infection, inflammation, or injury. (
  • This was accompanied by parallel alterations in endothelial activation and inflammation, marked respectively by de novo E-selectin expression in renal vascular endothelium and leukocyte adhesion to endothelium. (
  • A growing body of evidence suggests that renal inflammation is one of the key secondary processes that drive progression ( 1 - 5 ) and that vascular endothelial activation is an early and indispensable event in the recruitment of inflammatory cells to the renal parenchyma ( 6 - 8 ). (
  • Radiation and toxic chemicals cause "gap formation" between the cells of the vascular endothelium that makes it permeable to factor X, causing intense inflammation that explains sunburn. (
  • It is speculated that vascular inflammation, marked by activated monocytes and endothelium, plays a significant role in the pathophysiology of vaso-occlusion in sickle cell anemia. (
  • Coagulation does not occur in sunburn because gigantic factor VIII cannot penetrate the intact vascular endothelium. (
  • Only ACE inhibitor treatment normalised resistance vessel contractility and endothelium-dependent relaxation suggesting that factors other than blood pressure reduction play an important role in restoring resistance artery endothelial function. (
  • Few mechanistic studies, however, have examined the vascular effects of androgens in humans, although we have recently demonstrated an association between androgen deprivation and enhanced endothelial function in older men consistent with a deleterious effect of androgens on vascular reactivity. (
  • Kendrick J, Shah P, Andrews E, You Z, Nowak K, Pasch A, Chonchol M. Effect of Treatment of Metabolic Acidosis on Vascular Endothelial Function in Patients with CKD: A Pilot Randomized Cross-Over Study. (
  • Endothelial dysfunction , or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis . (
  • Since monocyte membrane linoleic acid content increases upon incubation with LDL, these results suggest that changes in the mechanical behavior of monocytes may occur during atherosclerosis promoting further monocyte adhesion to endothelium. (
  • We examined the expression of adhesion molecules such as endothelial-leukocyte adhesion molecule-1 (E-selectin), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), and the production of the proinflammatory cytokine interleukin-6 (IL-6). (
  • This is a method to visualise leukocyte adhesion to the endothelium in harvested pressurised vessels. (
  • Endothelial modulation was similar in both sets of arteries, suggesting that the endothelium does not mask an increased reactivity in 2-K, 1C hypertension. (
  • Anti-vascular endothelium (10) reactivity is stronger on capillary endothelium and weaker on larger arteries and veins. (
  • Graft endothelium is indeed the first barrier between self and non-self that is encountered by host lymphocytes upon reperfusion of vascularized solid transplants. (
  • Activated endothelium binds lymphocytes through a novel binding site in the alternately spliced domain of vascular cell adhesion molecule-1. (
  • Extravascular accumulation of specific subpopulations of T lymphocytes may be due to their preferential migration across the endothelium, their local differentiation once they have emigrated, or their enhanced survival, proliferation, or retention within tissues. (
  • Human Th2 cells, polarized and activated in vitro, express the chemokine receptor CCR2 more strongly and migrate across the endothelium to a greater degree than do similarly produced Th1 lymphocytes ( 5 ). (
  • Nuclear factor-kappa beta (NF-kβ) pro-inflammatory signalling is important in modulating endothelial dysfunction and may be important in vascular dysfunction associated with the ageing process. (
  • Early examination and treatment to dependent dysfunction of vascular endothelium. (
  • These findings suggest that IDH2 deficiency induces endothelial dysfunction through the induction of dynamic mitochondrial changes and impairment in vascular function. (
  • The results demonstrate that space-relevant irradiation induces a sustained vascular endothelial cell dysfunction. (
  • Endothelium dysfunction is believed to play a role in the development of cardiovascular disease. (
  • The aim of the present study was to evaluate the suitability of organ culture as a model for endothelium dysfunction. (
  • This shift in mediator profile resembles that in endothelium dysfunction. (
  • Organ culture provides an easily accessible model where the molecular changes that take place, when endothelium dysfunction is developed, can be examined over time. (
  • Endothelium dysfunction is developed in cardiovascular diseases such as arteriosclerosis, diabetes, congestive heart failure, coronary artery disease, stroke and hypertension (de Meyer & Herman 2000). (
  • In conducting arteries, the response to endothelium-dependent dilators declines when endothelium dysfunction is developed mainly due to a decrease in nitric oxide (NO) release. (
  • An injury to vascular endothelial cells (ECs) from pathogen or insult leads to endothelial dysfunction, which initiates the activation of two distinctly independent molecular pathways ( i.e., inflammatory and microthrombotic). (
  • DIT triggers vascular microthrombotic disease (VMTD), which manifestations include hypoxic multi-organ dysfunction syndrome, and thrombotic microangiopathy (TMA). (
  • Therefore, the proper functioning of the endothelium is important for the homeostasis of the body, and endothelial dysfunction is associated with several pathophysiological conditions, including atherosclerosis, hypertension, and diabetes [24]. (
  • Endothelial dysfunction is now regarded as an early marker of vascular disease and therefore an important target for therapeutic intervention and discovery of novel treatments. (
  • Vladimir R. Muzykantov, Ravi Radhakrishnan and David M. Eckmann, " Dynamic Factors Controlling Targeting Nanocarriers to Vascular Endothelium", Current Drug Metabolism (2012) 13: 70. (
  • Since arachidonic acid causes endothelium-dependent relaxations of coronary arteries through its metabolism to epoxyeicosatrienoic acids (EETs) by cytochrome P 450 , we wondered if the EETs represent EDHFs. (
  • Pilot Study to Investigate the Efficacy of L-arginine Therapy on Endothelium-dependent Vasodilation & Mitochondrial Metabolism in MELAS Syndrome. (
  • Treatment also prevented the development of impaired endothelium-dependent relaxation. (
  • These results suggest that atorvastatin can restore impaired endothelium-dependent vasodilations mediated by NO and EDHF but not hypotension in sepsis. (
  • The present study examined age-related changes in the vascular relaxation response to adenine nucleotides in hypertensive and normotensive rats. (
  • The extent of ATP-induced relaxation in aortic ring segments with intact endothelium was unchanged with advancing age. (
  • Rubbed (endothelium-denuded) ring preparations at the age of 4-6 weeks showed a dose-dependent relaxation similar to that of the unrubbed rings. (
  • ATP-induced relaxation may be manifested via the direct action on the vascular smooth muscle in young rats and may be altered through the response mediated by endothelium with advancing age. (
  • This suggests that the vascular smooth muscle of young rats has a P2-purinergic receptor leading to relaxation and that this receptor activity declines with advancing age. (
  • Endothelium-dependent relaxation was significantly greater in pregnant than in nonpregnant rats. (
  • 1 2 3 It is now recognized that EDRF is NO or a compound that releases NO. 4 Feletou and Vanhoutte 5 showed that acetylcholine causes endothelium-dependent hyperpolarization of coronary vascular smooth muscle that results in relaxation. (
  • We have recently reported that arachidonic acid causes endothelium-dependent relaxation of bovine coronary arteries. (
  • Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. (
  • Although anti-VEGF agents are widely used for cancer treatment, their use can also lead to vascular damage such as arterial thromboembolism and re-occlusion of new vessels. (
  • Comparable results were obtained in arterial endothelial cells and in endothelium stimulated with the cytokine tumor necrosis factor-α. (
  • Sodium overload stiffens vascular endothelial cells in vitro and promotes arterial hypertension in vivo. (
  • Arterial endothelium-derived hyperpolarization: potential role in pregnancy adaptations and complications. (
  • The vascular endothelium releases nitric oxide (NO) and von Willebrand Factor (VWF) in accord with autonomic balance to regulate the capillary gate mechanism that governs hemodynamic physiology and determines cardiac output, cardiac efficiency, tissue perfusion, tissue oxygenation, organ function, organ protection, and arterial patency. (
  • Knockout of PHD2 in EC was associated with vascular remodeling, as evidenced by an increase in pulmonary arterial media to lumen ratio and number of muscularized arterioles. (
  • To establish a cellular platform for studying endothelial biology, we have generated vascular endothelium from human induced pluripotent stem cells (iPSCs) exhibiting the rich functional phenotypic plasticity of mature primary vascular endothelium. (
  • Vascular endothelial cells (ECs) are exposed to hemodynamic forces, which modulate EC functions and vascular biology/pathobiology in health and disease. (
  • These cells have unique functions in vascular biology. (
  • 1 Division of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ), DKFZ-Center for Molecular Biology Alliance, 69120 Heidelberg, Germany. (
  • In view of the participation of vascular endothelial cells (EC) in a wide range of normal and pathological conditions, phenotypic heterogeneity of EC is an important concept for consideration: different sub-populations of EC may play differing biological roles in normal and patho-physiological states. (
  • Small physiological changes in extracellular sodium concentration directly stiffen vascular endothelium ( 16 ). (
  • The endothelium processes the entirety of the chemical composition to which the cardiovascular system is exposed, carrying out sophisticated computations that determine physiological output. (
  • It is the sensory interface for an enormous quantity of information about the chemical environment to which the vascular system is exposed and which provides cues on physiological status. (
  • Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of the adhesion receptor Gpr116/ADGRF5 has remained elusive. (
  • The chemicals are detected and processed selectively by the endothelium to direct resources that adjust physiological function. (
  • Vascular calcification is a regulated process that involves osteoprogenitor cells and frequently complicates common vascular disease, such as atherosclerosis and diabetic vasculopathy. (
  • Leukocyte transmigration through the vascular endothelium is a key step in the immune response, and also in progression of the cardiovascular disease atherosclerosis. (
  • XSC could regulate vascular activity factor and improve the function of endothelial dependent vascular dilation of patients with atherosclerosis. (
  • In addition, they may provide the foundation for novel therapies directed at a broad spectrum of vascular inflammatory disease states such atherosclerosis. (
  • Although it has been shown that excess vascular oxidative stress contributes to impaired EDRF action in experimental hypercholesterolemia and atherosclerosis, there are no data in literature related to antioxidant enzymes in intima bearing vessels predisposing to atherosclerosis. (
  • Sözmen E.Y., Kerry Z., Üstünes L., Uysal F., Özer A., Onat T. (1998) Variations of Endothelium Antioxidant Enzymes and Nitrite/Nitrate Levels in Collar-Induced Atherosclerosis of Rabbits. (
  • The alterations with age of P2-purinergic receptor in the vascular smooth muscle and endothelial cell are not affected by genetic hypertension. (
  • Methods: To specifically study the mechanism of anesthetic interaction with the nitric oxide-guanylyl cyclase pathway, cultured vascular smooth muscle and endothelial cell-vascular smooth muscle (EC-VSM) co-culture models were chosen. (
  • Sepsis has been reported to impair endothelium-dependent vasodilations mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). (
  • Eighteen hours after the induction of sepsis by cecal ligation and puncture, thoracic aorta and second generation pulmonary arteries were isolated to examine acetylcholine-induced endothelium-dependent dilations mediated by NO and EDHF, respectively. (
  • Endothelium-derived hyperpolarising factor (EDHF) was studied in the presence of 0.1 mM L-NOARG and indomethacin. (
  • EDHF is an endothelium-derived mediator, distinct from NO and prostaglandins, which hyperpolarises and relaxes smooth muscle cells. (
  • Although most agree that NO and EDHF are distinct entities, several articles indicate that NO also hyperpolarizes vascular smooth muscle and stimulates K + channel activity. (
  • Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. (
  • Bien que le monoxyde d'azote (NO) soit reconnu en tant que dilatateur dérivé de l'endothélium, il est bien établi aussi, particulièrement dans le système microvasculaire, qu'un autre facteur, le facteur hyperpolarisant dérivé de l'endothélium (EDHF), est un déterminant majeur du tonus vasodilatateur. (
  • Recent studies showed that high levels of transforming growth factor (TGF)-β1 in the airways reduced airway responsiveness, which was reversed in conditions of basic fibroblast growth factor (FGF2) deficiency, whereas high levels of vascular endothelial growth factor (VEGF) enhanced airway sensitization to allergens and airway hyperresponsiveness (AHR). (
  • To determine whether an intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) in eyes with diabetic macular edema (DME) affects the vascular infarction-related molecules (VIRMs). (
  • Molecular biological studies have shown that vascular endothelial growth factor (VEGF) is involved in the onset and progression of DME 3 , 4 , 5 , and clinical studies have shown that anti-VEGF therapy can resolve the DME. (
  • Propofol-induced damage to the blood-brain barrier endothelium evinces a vascular endothelial growth factor (VEGF) -dependent mechanism. (
  • Finally, vascular endothelial growth factor (VEGF), produced by mesenchymal stem cells (MSCs), makes ECs unresponsive to other proangiogenic stimuli. (
  • The vascular endothelium is a continuous network of about 10 trillion cells ( 1 ) that controls virtually all cardiovascular behavior. (
  • The endothelium is the single, innermost, layer of cells in blood vessels and it controls almost all cardiovascular functions. (
  • A healthy endothelium resists rupture and penetration from toxic elements (e.g. benzopyrene from tobacco smoke), and provides a slick, smooth surface for the easy and efficient passage of blood through the cardiovascular system. (
  • Our results demonstrate that iPSC-derived endothelium possesses a repertoire of functional phenotypic plasticity and is amenable to cell-based assays probing endothelial contributions to inflammatory and cardiovascular diseases. (
  • Ideal for both basic and clinical scientists, whether in industry or academia, and physicians, Vascular Endothelium in Human Physiology and Pathophysiology provides an up-to-date review of the vascular functions of the endothelium and its role in key areas of cardiovascular disease. (
  • Both naturally occurring and induced allo-antibodies directed to the Ag expressed on the membrane of EC are commonly found in renal recipients, and such antibodies, being capable of fixing the complement and damaging the tissues, are detrimental for the correct functioning of the endothelium ( 7 ). (
  • The recruitment of circulating leukocytes into inflamed tissues depends on interactions between adhesion molecules on leukocytes and vascular endothelial cells ( 11 , 12 , 13 , 14 , 15 ). (
  • 5-HT 1B receptor-mediated contraction was then compared in endothelium-intact and denuded vessels to evaluate the role of the endothelium in regulating sumatriptan-induced contractility in these tissues. (
  • The presence of an intact endothelium inhibited 5-HT 1B -induced contraction in both tissues. (
  • Surprisingly, in endothelial-denuded vascular tissues, l -NAME (100 μM) also significantly increased the maximal 5-HT 1B receptor-induced contraction in both tissues, with no effect on potency of sumatriptan. (
  • The "selectively permeable" vascular endothelium insulates tissue factor in extravascular tissues from Factor VII in flowing blood. (
  • Tissue factor in extravascular tissues slowly "leaks" through the vascular endothelium into flowing blood, where it activates factor VII to enable the continuous activities of factors VIII, IX, and X. (
  • Allograft endothelium is the first barrier between self and non-self in vascularized solid-organ transplantation, and preservation of its integrity and functions is mandatory to ensure a prolonged survival of the graft ( 5 ). (
  • Breakdown of the inner blood-retinal barrier and the blood-brain barrier is associated with changes in tight and adherens junction-associated proteins that link vascular endothelial cells. (
  • Endothelium lining the luminal surface of blood vessels is the key target and barrier for vascular drug delivery. (
  • This study tested a hypothesis that recovery of a vascular EC barrier after pathologic mechanical stress may be accelerated by cell exposure to physiologic CS levels and involves Rap1-dependent rearrangement of endothelial cell junctions. (
  • Taken together, our results demonstrate a prominent role of Rap1-mediated signaling mechanisms activated by low CS in acceleration of lung vascular EC barrier restoration. (
  • Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of white blood cells into and out of the bloodstream. (
  • 10 11 12 In addition, the production of NO by the blood vessel wall may limit intimal hyperplasia following local vascular injury by inhibiting smooth muscle proliferation and migration. (
  • We used an in vitro model of the blood vessel wall to test the premise that the vascular endothelium actively recruits circulating type 1 T cells to such lesions. (
  • Endothelium refers to cells that line the interior surface of blood vessels and lymphatic vessels , [1] forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. (
  • In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow. (
  • The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. (
  • In vitro investigations of the responses of vascular endothelium to fluid shear stress have typically been conducted under conditions where the time-mean shear stress is uniform. (
  • We analyzed the responses of hundreds of endothelial cells to carbachol (CCh) and adenosine triphosphate (ATP) and found that the endothelium segregates the responses to these two distinct components of the chemical environment into separate streams of complementary information that are processed in parallel. (
  • Possible involvement of endothelium-derived hyperpolarizing factor in vascular responses of abdominal aorta from pregnant rats. (
  • We evaluated Ang I and Ang II-mediated vascular responses and to correlate their contractile responses to the presence of endothelium and the protein levels of components of the RAS (AT 1 , AT 2 , Mas and ACE) in aorta isolated from genetically epileptic rats (WAR strain). (
  • A) Aortic wall (confocal microscopy, top 2 panels), and aortic endothelium () from wild type ( Mgp +/+ ) and Mgp − / − mice. (
  • To determine whether these mechanisms allow human leukocytes to effectively enter porcine grafts, the pathways by which human leukocytes adhere to TNF-α-stimulated porcine aortic endothelium were examined under static and physiologic flow conditions. (
  • Chlamydial and human HSP 60s therefore activate human vascular cell functions relevant to atherogenesis and lesional complications. (
  • It is concluded that antibody JC70 is of value for studying benign and malignant human vascular disorders in routinely processed tissue. (
  • We examined the effects of human interleukin 1 (IL-1) on the production of fibrinolytic components by cultured human vascular endothelium. (
  • Finally, as the response that follows transplantation has proven to be not necessarily destructive, the factors that foster graft endothelium functioning in spite of rejection, and how they could be therapeutically harnessed to promote long-term graft acceptance, are described: accommodation that is resistance of EC to donor-specific antibodies, and endothelial cell ability to induce Foxp3+ regulatory T-cells, that are crucial mediators of tolerance. (
  • Mouse anti-human monoclonal antibodies against vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin were obtained from Becton-Dickinson, and isotype mouse IgG1 and IgG2 not directed against endothelial cell antigens were obtained from ICN Immunobiologicals. (
  • These antibodies should prove useful for in vivo targeting to prostate cancer, as well as to the vascular compartment of a wide variety of carcinomas. (
  • Here, monoclonal antibodies against the extracellular domain of the vascular endothelial growth factor-C receptor that we have named VEGFR-3 were found to specifically stain endothelial cells of lymphatic vessels and vessels around tumors such as lymphoma and in situ breast carcinoma. (
  • Antibodies to tumor necrosis factor-alpha (TNF-α) and interleukin-1-beta (IL-1β) blocked activation of the endothelium by monocytes. (
  • There are some evidence linking excess vascular oxidative stress to the impairment of EDRF action associated with hypercholesterolemia. (
  • These results contribute to understanding how the endothelium can process large amounts of biochemical information for a coordinated, tissue-wide response. (
  • The effect of l -NAME after endothelial denudation may reflect the presence of a low density of residual endothelial cells as estimated by CD31 antibody staining combined with the modulating effect of nitric oxide released from nonendothelial cells in vascular tissue. (
  • The mechanism controlling occludin expression is similar to that which controls tissue-specific expression of the transferrin receptor in brain endothelium, leading to a scheme for endothelial differentiation, in which activation or repression of tissue-specific proteins is maintained by a set of transcription factors which include Sp3 and YY1. (
  • JC70: a new monoclonal antibody that detects vascular endothelium associated antigen on routinely processed tissue sections. (
  • Traumatic disruption as shown by the pink cells allows gigantic factor VIII to pass through the vascular endothelium and interact with tissue factor and factors VII, IX and X to initiate clot formation. (
  • The selectively permeable viscoelastic clot substitutes for the vascular endothelium and regulates the passage of factors VII and X to maintain optimal thrombin levels to energize tissue repair. (
  • Monoclonal antibody which specifically binds vascular endothelium tissue. (
  • This antibody reacts specifically with vascular endothelium and no other tissue. (
  • [4] Many considered the endothelium a specialized epithelial tissue. (
  • Reperfusion injury provoked a dramatic increase in adherent and emigrated leukocytes in the mesenteric vascular bed, associated with augmented tissue levels of myeloperoxidase. (
  • The vasodilator activity of α 1 -adrenoceptor agonists was tested in the rat mesenteric vascular bed (MVB), and the mechanism involved was investigated in cultured endothelial cells isolated from the bovine coronary vascular bed. (
  • Experimental observation of Chuanxiong and Chishao on reducing blood lipoid of hyperglycemia rats, anti-oxidation and vascular endothelium function. (
  • We investigated the effects of acute administration of a high concentration of lead acetate (100 µÌ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats . (
  • Ang II induced contractions in aortas from Wistar rats either with intact endothelium (E+) (1.16 ± 0.04 g, n = 6) and endothelium-denuded (E-) (1.24 ± 0.04 g, n = 6). (
  • These experiments have investigated how the endothelium modulates resistance artery contractility in hypertension. (
  • The balance of these biochemical and biomechanical stimuli critically regulates vascular function under physiologic and pathologic condition. (
  • However, it is not clear whether the vascular endothelium has a role in contributing osteoprogenitor cells to the calcific lesions. (
  • To determine whether the vascular endothelium contributes osteoprogenitor cells to vascular calcification. (
  • We show that enhanced BMP signaling in both types of mice stimulates the vascular endothelium to contribute osteoprogenitor cells to the vascular calcification. (
  • Our data suggest that the endothelium is a source of osteoprogenitor cells in vascular calcification that occurs in disorders with high BMP activation, such as deficiency of BMP-inhibitors and diabetes mellitus. (
  • Scale bar is 20 µm and applies to all images in panel B. Length of time after plating MDA-MB-231 cells on the endothelium is indicated in the upper right corner of each image in hour:minute:second format. (
  • Phase contrast (left) and DiIC 16 fluorescence (right) images of MDA-MB-231 cells plated onto an untreated HUVEC monolayer, at time points immediately after plating (top) and after 16 hours of interaction with the endothelium (bottom). (
  • As endothelial cells (EC) express a number of antigens (Ag) that are visible by the immune system of a genetically disparate individual, donor endothelium is invariably recognized by the host immune system, and therefore, it is the first and preferential target of the allo-immune response that follows organ transplantation without an adequate immunosuppression ( 6 ). (
  • In contrast, a P2-purinergic receptor leading to the generation of endothelium-derived relaxing factor may be activated in endothelial cells with advancing age. (
  • Lymphocyte extravasation involves multiple adhesion molecules that mediate lymphocyte binding to endothelial cells lining vascular beds. (
  • Here we (i) characterise NF-kβ signalling in vascular endothelial cells and examine the potential for CaMKII modulation and (ii) determine whether CaMKIIδ expression is altered in ageing. (
  • Therefore, these results indicate that Mokuboito and its constituents exert both vasodilating actions mediated by endothelium-dependent mechanisms (PGI 2 and NO from endothelium) and by endothelium-independent mechanisms (Ca 2+ influx control on smooth muscle cells). (
  • These findings demonstrate that nanomolar concentrations of phenylephrine, which are devoid of any contractile effect, induced a slight endothelium-dependent vasorelaxation in the rat MVB through the stimulation of α 1D -adrenoceptors, located on endothelial cells, which act through phospholipase C stimulation, followed by IP 1 generation, and nitric-oxide synthase activation. (
  • Chemical (acetylcholine) activation triggered spatiotemporally-complex, propagating IP3-mediated Ca2+ waves that originated in clusters of cells and progressed from there across the endothelium. (
  • Vascular cell adhesion molecule-1 (VCAM-1) is induced on endothelial cells by inflammatory cytokines, and binds mononuclear leukocytes through the integrin very late antigen-4 (VLA-4) (alpha 4 beta 1). (
  • We showed that this molecule, which we named lymphocyte-vascular adhesion protein 2 (L-VAP-2), mediates lymphocyte adhesion to cultured endothelial cells. (
  • Interestingly, the spindle cells of several cutaneous nodular AIDS-associated Kaposi's sarcomas and the endothelium around the nodules were also VEGFR-3 positive. (
  • To regulate function, the endothelium continuously monitors multiple chemicals that are circulating in the blood or derived from nearby cells (e.g. endocrine, paracrine, autocrine or neurotransmitter signals). (
  • To monitor the behaviour of the endothelium, changes in endothelial cytosolic Ca2+ concentration were measured in ~200 endothelial cells in small mesenteric arteries using the indicator Cal-520 and high-resolution imaging. (
  • 5 In vascular cells, this oxidative reaction is mediated by two distinct classes of NOS. (
  • A constitutively active Ca 2+ -calmodulin-dependent isoform of the enzyme predominates in endothelial cells, whereas a Ca 2 -insensitive isoform is induced by inflammatory cytokines in vascular smooth muscle. (
  • 6 7 8 9 In the circulation, the release of NO by vascular cells plays an important role in regulating blood flow by inhibiting vascular tone and platelet adhesion and aggregation. (
  • Both the cytokine-stimulated release of NO by vascular smooth muscle cells and the NO-induced vascular hyporeactivity following endotoxin administration can be prevented by eliminating l -arginine from the extracellular environment. (
  • 8 16 In addition, the recent finding that an inhibitor of l -arginine uptake, l -lysine, blocks IL-β-stimulated NO production by vascular smooth muscle cells suggests that l -arginine transport can become the rate-limiting step in NO synthesis by these cells. (
  • However, the function of IDH2 in vascular endothelial cells is mostly unknown. (
  • In this study the effects of IDH2 deficiency on mitochondrial and vascular function were investigated in endothelial cells. (
  • TNF-α, IL-1β) to activate renal vascular endothelial cells, causing them to transit to a proinflammatory phenotype ( 9 ). (
  • Very late antigen-4 and CD11/CD18 integrins mediated passage of the T cells across both resting and stimulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattractant protein 1) was responsible for the enhanced migration of T cells across stimulated HUVEC. (
  • These results suggest that the vascular endothelium may contribute to the selective accumulation of type 1 T cells in certain pathological lesions, including those of Lyme disease. (
  • Endothelial cells as vascular salt sensors. (
  • The in vitro culture of endothelial cells (ECs) is an indispensable tool for studying the role of the endothelium in physical and pathological conditions. (
  • So far, this model for vascular disease has only been applied to study the phenotypic changes of smooth muscle cells. (
  • Molecules and structures involved in the adhesion of natural killer cells to vascular endothelium. (
  • The present study was designed to define molecules and structures involved in the interaction of natural killer (NK) cells with the vascular endothelium in vitro. (
  • In addition to the CD18-CD11a/intercellular adhesion molecule pathway, the interaction of resting or IL-2-activated NK cells to IL-1-activated EC involved the VLA-4 (alpha 4 beta 1)-vascular cell adhesion molecule 1 receptor/counter-receptor pair. (
  • Localization of anticoagulantly active heparan sulfate proteoglycans in vascular endothelium: antithrombin binding on cultured endothelial cells and perfused rat aorta. (
  • The anticoagulantly active HSPG were concentrated immediately beneath the aortic and vasa vasorum endothelium with only a very small extent of labeling noted on the luminal surface of the endothelial cells. (
  • Functional vascular endothelium derived from human induced pluripotent stem cells. (
  • Human genotype-phenotype studies of endothelium are limited by the unavailability of patient-specific endothelial cells. (
  • The vascular endothelium is a diaphanous layer of specialized cells, one cell thick, that lines the inner surface of all blood vessels and is the sole constituent of capillaries. (
  • The loosely bound cells of the hepatic vascular endothelium facilitate glucuronidation of toxic substances and lipoprotein processing. (
  • The vascular endothelium is "selectively permeable" as shown in the green cells. (
  • The cells of the vascular endothelium react to local conditions and communicate with one another via electrical signals, so that direct innervation of every cell is unnecessary. (
  • The pericyte coverage and vascular smooth muscle cells were also significantly increased in the PA. (
  • Endothelial cells release a variety of compounds that regulate vascular tone, including prostacyclin, EDRF, and endothelin. (
  • A combination of aged garlic extract and coenzyme Q10 may improve vascular health by improving the function of the cells lining the blood vessels, says a new study with LA County firefighters. (
  • Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells. (
  • Vascular endothelial cells line the entire circulatory system , from the heart to the smallest capillaries . (
  • Endothelial cells express enzymes that produce ROS in response to various stimuli, and H 2 O 2 is a potent relaxant of vascular smooth muscle. (
  • Because BDNF is created by healthy vascular endothelial cells. (
  • To assess if an impaired cross-talk between endothelial cells (ECs) and perivascular/multipotent mesenchymal stem cells (MSCs) might induce a perturbation of vascular repair and leading to a phenotypic switch of MSC toward myofibroblast in Systemic Sclerosis (SSc). (
  • Endothelium is a single layer of squamous endothelial cells that line the interior surface of blood vessels, and lymphatic vessels. (
  • The endothelium is a thin layer of single flat (squamous) cells that line the interior surface of blood vessels and lymphatic vessels. (
  • Since both prostacyclin and the EETs relax coronary arteries, 24 26 27 they were proposed to mediate the endothelium-dependent relaxations induced by arachidonic acid. (
  • H 2 O 2 itself can mediate endothelium-dependent relaxations in some vascular beds. (
  • Acetylcholine (ACh) is commonly used to assess endothelium-dependent dilatation. (
  • Cancer cell migration through the endothelium and into the basement membrane represents a critical step in the metastatic cascade, yet it is not well understood. (
  • Le peroxyde d'hydrogène (H 2 O 2 ), en particulier, peut entraîner la prolifération des myocytes vasculaires (et, de manière incongrue, l'apoptose), l'hyperplasie, l'adhésion et la migration des cellules ainsi que la régulation du tonus musculaire lisse. (
  • It is hypothesized that monocytes are activated in sickle cell disease and can enhance vaso-occlusion by activating endothelium. (
  • Cell-to-cell contact of monocytes and endothelium enhanced, but was not required for, activation. (
  • Endothelial modulation was specific to 5-HT 1B receptors because removal of the endothelium did not significantly alter contraction to norepinephrine, histamine, prostaglandin, or potassium chloride in the saphenous vein or basilar artery. (
  • Nevertheless, the host immune response that follows recognition of EC allo-Ag is not necessarily destructive, in spite of graft rejection, accommodation, where not active tolerance, may operationally establish, thus fostering the endothelium to fulfill its functions ( 5 ). (
  • Therefore, much of the knowledge on properties and functions of the vascular endothelium has been obtained from primary EC cultures. (
  • Treatment of SHRs with either an ACE inhibitor, a vasodilator or a calcium antagonist prevented the rise in blood pressure and normalised vascular structural alterations. (
  • There was a positive correlation between blood pressure and vascular structure, suggesting that blood pressure is a major determinant of vascular structure. (
  • The technique enables studying vascular adhesion under shear flow with differing intraluminal pressures up to 200 mmHg thus mimic-ing the pathophysiological conditions of high blood pressure. (
  • Dynamic parameters of the vasculature including the blood hydrodynamics as well as surface density, accessibility, membrane mobility and clustering of target determinants modulate these phases of the targeting, especially anchoring to endothelium. (
  • Vascular Endothelium is the single cell layer that lines the inner surface of blood vessels. (
  • The vascular endothelium comprises a dynamic interface with the blood and acts as an integrator and transducer of both biochemical (e.g. inflammatory cytokines) and biomechanical (e.g. laminar shear stress) stimuli. (
  • A combination of HMB (a metabolite of leucine), glutamine and arginine may improve vascular function and blood flow in older people, says a new study. (
  • Shear stress--which is caused by blood flow over the lining of our blood vessels--activates the endothelium, and allows for BDNF secretion. (
  • This historic 1915 paper by Stockard describes blood and vascular endothelium in embryos. (
  • The endothelium normally provides a surface on which blood does not clot, because it contains and expresses substances that prevent clotting, including heparan sulfate which acts as a cofactor for activating antithrombin, a protease that inactivates several factors in the coagulation cascade. (
  • CD49d/CD29) that binds to VCAM-1 (CD106) expressed by cytokine-activated endothelium. (
  • Cerebral cavernous malformations form an anticoagulant vascular domain in humans and mice. (
  • A role for the endothelium in vascular calcification. (
  • These findings demonstrate a critical role for endogenous NO as a negative regulator of vascular smooth muscle proliferation in response to a remodeling stimulus. (
  • New pharmacological therapies are evolving from our understanding of the role of the endothelium. (
  • The present study examined the role of endothelial cell specific prolyl hydroxylase-2 (PHD2) in the development of PAH and pulmonary vascular remodeling. (
  • Endothelium impairs the contractile response induced by Angiotensin in WAR, suggesting that endothelial relaxing factors play important role on the aorta contraction. (
  • Over the past two decades, investigators have increasingly recognized the importance of the endothelium as a central regulator of vascular and body homeostasis. (
  • Based on these observations, we hypothesize that KLF4 may serve as a critical transcriptional regulator of endothelial cell function and vascular homeostasis. (
  • Putative endothelial sources of H 2 O 2 and the effects of H 2 O 2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. (
  • Here, we used a previously established in vitro model of the endothelium and live cell imaging, in order to observe cancer cell transmigration and compare this process to leukocytes. (
  • VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration. (
  • Much work has previously focused on the biological aspects of leukocyte transmigration, such as cytokine exposure, junctional protein organization in the endothelium, and signaling pathways. (
  • OBJECTIVE To evaluate whether the administration of metformin exerts any effects on serum homocysteine (Hcy) levels in patients with polycystic ovary syndrome (PCOS) and whether supplementation with folate enhances the positive effects of metformin on the structure and function of the vascular endothelium. (
  • Based on these considerations, the aim of the present study was to evaluate whether the administration of metformin exerts any effect on serum Hcy levels in patients with PCOS and whether supplementation with folate enhances the positive effects of metformin on the structure and function of the vascular endothelium. (
  • Our data suggest that it also has a function in mediating lymphocyte adhesion to the endothelium. (
  • In this review, we have firstly described the current understanding of the structure of CRP, its function, and interaction with the vascular endothelial cell. (
  • The last decade, it became increasingly apparent that ECs display significant heterogeneity in phenotype, function, antigenic composition and biological behavior depending on the vascular system they originate from. (
  • Our understanding of the vital function of the vascular endothelium in circulatory physiology is rapidly expanding. (
  • This plasticity is critical for vascular function and when dysregulated is pathogenic in several diseases. (
  • In line with cardiac remodelling, vascular structure and function are altered following training, but little is known about peripheral vascular adaptations in HCM. (
  • Although it has been reported that Angiotensin II (Ang II) release and Angiotensin receptors expression are altered in many cerebral areas in patients/animal models with neurological disorders, there are no data on the vascular function. (
  • The first specific molecular marker for the lymphatic endothelium should provide a useful tool for the analysis of lymphatic vessels in malignant tumors and their metastases and the cellular origin and differentiation of Kaposi's sarcomas. (
  • Endothelium lines the inner wall of vessels, shown here. (
  • Lymphocyte attachment to porcine endothelium was primarily L-selectin mediated, whereas β 2 integrin and VCAM-1/very late Ag-4 (VLA-4) interactions promoted static adhesion. (
  • CD73 is involved in lymphocyte binding to the endothelium: characterization of lymphocyte-vascular adhesion protein 2 identifies it as CD73. (