Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Endothelium: A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.Endothelium, Corneal: Single layer of large flattened cells covering the surface of the cornea.Endothelium, Lymphatic: 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.Endothelial Cells: 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.Cell Adhesion: Adherence of cells to surfaces or to other cells.Nitric Oxide: 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.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Cells, Cultured: 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.Aorta: The main trunk of the systemic arteries.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Umbilical Veins: 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.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Vasoconstriction: The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.Intercellular Adhesion Molecule-1: 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.Vascular Cell Adhesion Molecule-1: 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)Capillaries: The minute vessels that connect the arterioles and venules.Microcirculation: The circulation of the BLOOD through the MICROVASCULAR NETWORK.Arteries: The vessels carrying blood away from the heart.Acetylcholine: 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.Cell Adhesion Molecules: 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.E-Selectin: 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.Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Rabbits: 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.Cornea: 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)Vasoconstrictor Agents: Drugs used to cause constriction of the blood vessels.Leukocytes: White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).Nitric Oxide Synthase Type III: A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.Biological Factors: Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.Nitric Oxide Synthase: An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.P-Selectin: Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.Muscle Relaxation: That phase of a muscle twitch during which a muscle returns to a resting position.Capillary Permeability: 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.Descemet Membrane: 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.Blood Vessels: Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines.Leukocyte Rolling: 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)Cell Movement: The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins.Coronary Vessels: The veins and arteries of the HEART.Nitroarginine: 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)Antigens, CD31: 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.Corneal Transplantation: Partial or total replacement of the CORNEA from one human or animal to another.Indomethacin: 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.Hemangioblasts: Bipotential angio-hematopoietic stem cells that give rise to both HEMATOPOIETIC STEM CELLS and ENDOTHELIAL CELLS.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Methylene Blue: 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.Nitroprusside: 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.Neutrophils: 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.Mice, Inbred C57BLArterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries.Stress, Mechanical: 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.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Cattle: 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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Microscopy, Electron, Scanning: 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.Antigens, CD18: 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.Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.Arginine: An essential amino acid that is physiologically active in the L-form.Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.Microscopy, Electron: 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.Human Umbilical Vein Endothelial Cells: Endothelial cells that line venous vessels of the UMBILICAL CORD.Rats, Sprague-Dawley: 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.Endothelins: 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.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Swine: 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).Epoprostenol: 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).L-Selectin: Cell adhesion molecule and CD antigen that serves as a homing receptor for lymphocytes to lymph node high endothelial venules.RNA, Messenger: 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.Endothelium-Dependent Relaxing Factors: Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.Bradykinin: 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.Muscle Contraction: 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.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Transendothelial and Transepithelial Migration: 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.Hemorheology: The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Signal Transduction: 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: 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.Selectins: 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.Norepinephrine: 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.Monocytes: 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.Cell Communication: 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.Veins: The vessels carrying blood away from the capillary beds.Glycocalyx: 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)Potassium Chloride: 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.Microvessels: The finer blood vessels of the vasculature that are generally less than 100 microns in internal diameter.Blood-Brain Barrier: 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.Cyclic GMP: 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)Inflammation: 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.Mice, Knockout: 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.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Lymphatic System: A system of organs and tissues that process and transport immune cells and LYMPH.omega-N-Methylarginine: A competitive inhibitor of nitric oxide synthetase.Tumor Necrosis Factor-alpha: 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.Neovascularization, Physiologic: The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.Neovascularization, Pathologic: A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.Intercellular Junctions: 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)Fuchs' Endothelial Dystrophy: 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.Vasomotor System: The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.Antigens, CD: 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.Chemotaxis, Leukocyte: The movement of leukocytes in response to a chemical concentration gradient or to products formed in an immunologic reaction.15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid: 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)Arteriosclerosis: 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.Splanchnic Circulation: The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.von Willebrand Factor: 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.Dogs: 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)Endothelin-1: 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)Lymphocyte Function-Associated Antigen-1: 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.Carotid Arteries: 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.Corneal Diseases: Diseases of the cornea.Corneal Edema: An excessive amount of fluid in the cornea due to damage of the epithelium or endothelium causing decreased visual acuity.Disease Models, Animal: 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.Receptor, TIE-2: 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).Rats, Inbred WKY: A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Microscopy, Confocal: 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.Vascular Endothelial Growth Factor A: 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.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Receptors, Lymphocyte Homing: 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.Integrins: 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.Vascular Resistance: 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.Thrombomodulin: 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.Up-Regulation: 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.Calcimycin: 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.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Endocardium: The innermost layer of the heart, comprised of endothelial cells.Thrombin: An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.Fluorescent Antibody Technique: 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.Cyclooxygenase Inhibitors: 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.Muscle Tonus: 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)Blotting, Western: 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.Erythrocytes, Abnormal: Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.Mesenteric Veins: 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.Calcium: 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.Rats, Inbred Strains: 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.Eye Banks: Centers for storing various parts of the eye for future use.Vasculitis: Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.Fluorescent Antibody Technique, Indirect: 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)Flow Cytometry: 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.Lymphatic Vessels: Tubular vessels that are involved in the transport of LYMPH and LYMPHOCYTES.Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the ABDOMINAL WALL and conveys their blood vessels and nerves.Receptors, Cell Surface: 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.Charybdotoxin: A 37-amino acid residue peptide isolated from the scorpion Leiurus quinquestriatus hebraeus. It is a neurotoxin that inhibits calcium activated potassium channels.Corneal Stroma: The lamellated connective tissue constituting the thickest layer of the cornea between the Bowman and Descemet membranes.Iris Diseases: Diseases, dysfunctions, or disorders of or located in the iris.Receptors, Leukocyte-Adhesion: 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.Immunoenzyme Techniques: 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.Platelet Adhesiveness: The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.Tissue Preservation: 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).Cerebral Arteries: The arterial blood vessels supplying the CEREBRUM.Basilar Artery: 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.Cell Count: The number of CELLS of a specific kind, usually measured per unit volume or area of sample.Gene Expression Regulation: 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.Superoxides: 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.Tissue Distribution: 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.Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.Anoxia: Relatively complete absence of oxygen in one or more tissues.Reverse Transcriptase Polymerase Chain Reaction: 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.Interleukin-1: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Aqueous Humor: 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)Cell Membrane Permeability: A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.Microscopy, Fluorescence: 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.Membrane Proteins: 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.Serotonin: 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.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Shear Strength: 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.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Culture Techniques: 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.Saphenous Vein: The vein which drains the foot and leg.Vascular Diseases: 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.OxadiazolesMice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery.Endothelial Growth Factors: 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.Antigens, CD11: 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.Myography: The recording of muscular movements. The apparatus is called a myograph, the record or tracing, a myogram. (From Stedman, 25th ed)Vascular Endothelial Growth Factor Receptor-3: 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.Nitric Oxide Donors: 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)Rheology: 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.In Situ Hybridization: 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.Brain: 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.Thromboxane A2: 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).Pulmonary Circulation: The circulation of the BLOOD through the LUNGS.Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Molecular Sequence Data: 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.Lymphocytes: 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.Dinoprost: 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.Epithelium: One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.Substance P: 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.Caveolin 1: 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.Anemia, Sickle Cell: 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.Methoxamine: An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.Antibodies: 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).Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.Histamine: 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.Coculture Techniques: 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.

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)

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.
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 ...
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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 ...
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 ...
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 ...
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, ...
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 ...
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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. ...
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.
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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.
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 ...
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 ...
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 ...
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 ...
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 ...
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 ...
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 ...
Vascular lesions[edit]. These result from injury to the vascular endothelium. Causes:. Venoocclusive disease: Chemotherapeutic ...
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 ...
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 ... The organization of the endocardial endothelium and the intercellular cleft help to establish the blood-heart barrier by ... Most notably, intercellular clefts are found between epithelial cells and the endothelium of blood vessels and lymphatic ...
Endothelium dysfunction is a prototypical characteristic of vascular disease, common in patients with autoimmune diseases such ... 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 ...
"Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives". Physiological Reviews. ...
Stasis: Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium. *Common causes ... Vascular surgery. A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in ... Organization and recanalization involves the ingrowth of smooth muscle cells, fibroblasts and endothelium into the fibrin-rich ... Platelet activation occurs through injuries that damage the endothelium of the blood vessels, exposing the enzyme called factor ...
In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium. Along with acting as a semi- ... the endothelium is responsible for maintaining vascular tone and regulating oxidative stress by releasing mediators, such as ... Endothelial dysfunction may be involved in the development of atherosclerosis[3][4] and may predate vascular pathology.[3][5] ... Kuvin JT, Mammen A, Mooney P, Alsheikh-Ali AA, Karas RH (Feb 2007). "Assessment of peripheral vascular endothelial function in ...
"Vascular endothelium: the battlefield of dengue viruses". Wiley Online Library. 53 (3): 287-299. doi:10.1111/j.1574-695X. ...
Pericyte Mesoderm Endothelium Cossu, G; Bianco, P (2003). "Mesoangioblasts--vascular progenitors for extravascular mesodermal ...
Annals of Vascular Surgery, 20(5), 653-58 *^ a b c Thornalley, P. J. (2005). The potential role of thiamine (vitamin B1) in ... 2006). Thiamine (vitamin B-1) improves endothelium-dependent vasodilatation in the presence of hyperglycemia. ... Peripheral vascular disease, which contributes to intermittent claudication (exertion-related leg and foot pain) as well as ... 2003). "Oral L-arginine and vitamins E and C improve endothelial function in women with type 2 diabetes". Vascular Medicine. 8 ...
Increase intracellular calcium in vascular endothelium. *increased endocrine and exocrine gland secretions, e.g. salivary ... Indeed, direct stimulation of vascular smooth muscle, M3 mediates vasconstriction in pathologies wherein the vascular ... activation of M3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular ... endothelium is disrupted.[22] The M3 receptors are also located in many glands, which help to stimulate secretion in, for ...
"A role for the endothelium in vascular calcification". Circ. Res. 113 (5): 495-504. doi:10.1161/CIRCRESAHA.113.301792. PMC ... The protein acts as an inhibitor of vascular mineralization and plays a role in bone organization. MGP is found in number body ...
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 ...
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 ...
... 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 ...
Evolutionary origins of the blood vascular system and endothelium. Journal of Thrombosis and Haemostasis 11 (s1): 46-66. Bailey ... 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 ... Vascular surgeons focus on other parts of the circulatory system. Diseases affecting the cardiovascular system are called ...
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., ...
The regulation of vascular tone in the endothelium of blood vessels is mediated by purinergic signalling. A decreased ... and Vascular Biology. 32 (4): 845-850. doi:10.1161/atvbaha.111.226803. PMID 22423035. Lu, D.; Insel, P. A. (18 December 2013 ... and Vascular Biology. 32 (4): 879-886. doi:10.1161/atvbaha.111.226878. Mortaz, Esmaeil; Folkerts, Gert; Nijkamp, Frans P.; ... and Vascular Biology. 32 (4): 856-864. doi:10.1161/atvbaha.111.226845. PMC 3353547 . PMID 22423037. Eltzschig, Holger K.; ...
These result from injury to the vascular endothelium.. Causes:. Venoocclusive disease: Chemotherapeutic agents, bush tea. ...
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 ...
Shibuya N, Mikami Y, Kimura Y, Nagahara N, Kimura H (November 2009). "Vascular endothelium expresses 3-mercaptopyruvate ...
Monahan‐Earley, R., Dvorak, A. M., & Aird, W. C. (2013). Evolutionary origins of the blood vascular system and endothelium. ... The circulatory system, also called the cardiovascular system or the vascular system, is an organ system that permits blood to ... Vascular surgeons focus on other parts of the circulatory system. Cardiovascular disease. Main article: Cardiovascular disease ... The blood vascular system first appeared probably in an ancestor of the triploblasts over 600 million years ago, overcoming the ...
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 ...
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 https://doi.org/10.1007/978-1-4615 ...
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 ...
Circular Noncoding RNA HIPK3 Mediates Retinal Vascular Dysfunction in Diabetes Mellitus Kun Shan, Chang Liu, Bai-Hui Liu, Xue ...
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 ...
Vascular Cell Senescence Contributes to Blood-Brain Barrier Breakdown Yu Yamazaki, Darren J. Baker, Masaya Tachibana, Chia-Chen ... Differential Effect of B-Vitamin Therapy by Antiplatelet Use on Risk of Recurrent Vascular Events After Stroke Baback Arshi, ...
... 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 ...
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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. ...
More From BioPortfolio on "A Study of Niaspan on Endothelium-Dependent and Endothelium-Independent Vascular Reactivity". * ... A Study of Niaspan on Endothelium-Dependent and Endothelium-Independent Vascular Reactivity. 2014-07-23 21:09:32 , BioPortfolio ... A Study of Niaspan on Endothelium-Dependent and Endothelium-Independent Vascular Reactivity ...
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 ...
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 ...
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 ...
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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 ...
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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 ...
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  • It is concluded that antibody JC70 is of value for studying benign and malignant human vascular disorders in routinely processed tissue. (bmj.com)
  • In addition, DHE and DCF fluorescence staining demonstrated that IL-4 increases ROS production in human vascular endothelial cells. (vt.edu)
  • We have also provided the first novel evidence that 5-LOX, one of the enzymes associated with arachidonic acid metabolism, is responsible for the IL-4-induced ROS generation and MCP-1 expression in human vascular endothelial cells. (vt.edu)
  • We examined the effects of human interleukin 1 (IL-1) on the production of fibrinolytic components by cultured human vascular endothelium. (scripps.edu)
  • Human vascular endothelial cell lines, including retinal (three lines from three different donors), aortic, umbilical vein, and dermal microvascular endothelium, as well as human foreskin fibroblasts, were grown to confluence in 24-well plates. (elsevier.com)
  • 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. (nih.gov)
  • Conclusion and implication: These results suggest that the endothelium in rat mesenteric arteries regulates and maintains vascular tone via counteracting not only vasoconstriction through releasing endothelium-derived relaxing factors, but also vasodilatation, in part by releasing an EDCF, thromboxane A 2 . (elsevier.com)
  • Regulation of vascular tone during pregnancy: a novel role for the pregnane X receptor. (semanticscholar.org)
  • It is involved in the regulation of vascular tone, local hemostasis, proliferation. (ssmj.ru)
  • 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. (wikipedia.org)
  • Experimental observation of Chuanxiong and Chishao on reducing blood lipoid of hyperglycemia rats, anti-oxidation and vascular endothelium function. (springer.com)
  • 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 . (bvsalud.org)
  • A) Aortic wall (confocal microscopy, top 2 panels), and aortic endothelium () from wild type ( Mgp +/+ ) and Mgp − / − mice. (nih.gov)
  • Endothelium-dependent vasorelaxation was impaired, and the concentration of bioavailable NO decreased in the aortic ring in IDH2 knockout mice. (ovid.com)
  • 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. (rupress.org)
  • Tachyzoites showed higher [ 3 H]-uracil incorporation after incubation with retinal vascular endothelial cells in comparison with aortic (55% more), umbilical vein (33% more) and dermal (34% more) endothelial cells. (elsevier.com)
  • 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. (springer.com)
  • Small physiological changes in extracellular sodium concentration directly stiffen vascular endothelium ( 16 ). (pnas.org)
  • Vascular theory of the glaucomatous optic neuropathy pathogenesis: physiological and pathophysiological rationale: Part 2. (ssmj.ru)
  • 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. (ahajournals.org)
  • 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. (ahajournals.org)
  • Recent studies have shown the restoration of endothelial function before significant reduction of serum cholesterol levels effect of statins on the endothelium were first defined by their ability to enhance endothelial NO production, upregulating endothelial nitric oxide synthase (eNOS) PI3 kinase/Akt signaling, which is a crucial regulator of cell metabolism and apoptosis, appears to mediate statin-induced eNOS upregulation. (pharmaceuticalintelligence.com)
  • Tocotrienol rich tocomin, which prevented the diet-induced changes in vascular function, reduced vascular superoxide production and abolished the diet-induced changes in eNOS and other protein expression. (frontiersin.org)
  • In this study, we use 2 mouse models of vascular calcification, mice with gene deletion of matrix Gla protein, a bone morphogenetic protein (BMP)-inhibitor, and Ins2Akita/+ mice, a diabetes model. (nih.gov)
  • 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. (bl.uk)
  • 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. (ahajournals.org)
  • Recent studies indicate that NO synthesis by vascular smooth muscle is strictly dependent on the presence of extracellular l -arginine. (ahajournals.org)
  • 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. (ahajournals.org)
  • 5 Since NO generation by vascular smooth muscle and by endothelium has contrasting requirements for extracellular l -arginine, the present study directly compared l -arginine transport by these different cell types cultured from the same vascular source, specifically BASMCs and BAECs. (ahajournals.org)