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Details for anatomical structure: vascularendothelial cell

EndoNet ID: ENC00150

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Synonyms

vascularendothelial cell, ,

Links to other resources

Cytomer cy0052346

Larger structures

    Substructures

      Secreted hormones

      • Hormone: RANTES

      • Hormone: VCAM1 soluble form

      • Hormone: PDGFD

      • Hormone: osteopontin

      • Hormone: FGF-2

      • Hormone: sALCAM

      • Hormone: elastase-2

      • Hormone: soluble E-selectin

      • Hormone: slit-2 isoform 1 C-product

      • Hormone: slit-2 isoform 1 N-product

      Receptors

      • Receptor: neuropilin-2

        • Neuropilin expression and function in epithelial cells has received little attention when compared with neuronal and endothelial cells [2]

        Induced phenotype:

        • regulation of angiogenesis
          • neuropilin-1 (NRP1) and neuropilin-2 (NRP2) play essential roles in axonal growth and guidance and in physiological and pathological angiogenesis [2]

      • Receptor: ER-beta

        Induced phenotype:

        • positive regulation of angiogenesis
          • Estradiol is known to promote angiogenesis in several tissues. [3]
          • ER-beta-knockout mice demonstrated abnormal vascular function and hypertension, increased mortality, and aggravation of heart failure. [4]

      • Receptor: leptin receptor isoform b

        Induced phenotype:

        • positive regulation of vasodilation
          • Leptin is a vasodilator in the peripheral vasculature in vitro. [5]
          • Leptin mediates nitric oxide-dependent vasodilatation in rat superior superior mesenteric artery rings. [6]

      • Receptor: PLXND1

      • Receptor: TNFRSF12A

        Induced phenotype:

        • positive regulation of cell proliferation
          • TNFSF12 has a role in vasculature formation in vivo. [7]
          • TNFSF12 induces proliferation of endothelial cells in vitro and acts as a potent inducer of angiogenesis in a rat cornea pocket angiogenesis assay. [7]

      • Receptor: Vascular endothelial growth factor receptor 1

        Induced phenotype:

        • vasculogenesis
          • VEGF is a crucial regulator of vasculogenesis. [8]
        • vascular permeability
          • VEGF is a crucial regulator of vascular permeability. [8]

      • Receptor: sVEGF-R1

      • Receptor: hepatocyte growth factor receptor

      • Receptor: E-selectin

      • Receptor: P-selectin

      • Receptor: Lysophosphatidic acid receptor 3

        Induced phenotype:

        • negative regulation of apoptosis
          • S1P protects VECs from serum-deprived apoptosis by nitric oxide production through S1P3 receptor. [9]

      • Receptor: Lysophosphatidic acid receptor 1

        Induced phenotype:

        • positive regulation of angiogenesis
          • LPA is a mediator in angiogenesis. An initial characterization of knockout mice revealed the presence of frontal cephalic hemorrhages in Lpar1-deficient mice. [10]
        • cell maturation
          • LPA is a mediator in vascular maturation. An initial characterization of knockout mice revealed the presence of frontal cephalic hemorrhages in Lpar1-deficient mice. [10]
        • induction of cytokine expression
          • Lysophosphatidic acid induces expression of cytokines (MCP-1, IL-8, IL-1β) in vascular endothelial cells. [11]
          • Expression of inflammatory cytokines play important role in development of atherosclerosis and thrombosis. [11]
        • negative regulation of apoptosis
          • S1P protects VECs from serum-deprived apoptosis by nitric oxide production through S1P1 receptor. [9]

      • Receptor: Lysophosphatidic acid receptor 2

      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • regulation of cardiovascular system
          • S1P was also shown to regulate the cardiovascular system; intravenous administration of S1P decreased heart rates, ventricular contraction, and blood pressure in rats. [12]
        • positive regulation of blood vessel endothelial cell migration
          • S1P induces migration of VECs. [13]
          • S1P receptor-mediated signaling plays a major regulatory role in angiogenesis. [14]
          • VEC migration is inhibited by antisense oligonucleotides against s1p1. [15]
        • positive regulation of endothelial cell proliferation
          • S1P induces proliferation of VECs. [16]
          • S1P receptor-mediated signaling plays a major regulatory role in angiogenesis. [14]
        • positive regulation of angiogenesis
          • S1P1 plays a primary role in angiogenesis by its potent activation of Rac, potentially through the intimate interplay with PDGF. [13]
        • adherens junction assembly
          • S1P-induced VEC adherens junction assembly and cell barrier integrity are blocked by antisense oligonucleotides against s1p1. [17]
          • Expression of a dominant negative S1P1 mutant inhibits S1P-induced VEC assembly and migration. [13]
          • S1P stimulates the formation and maintenance of VECs assembly/integrity by activating S1P1. [18]

      • Receptor: Sphingosine 1-phosphate receptor 3

        Induced phenotype:

        • positive regulation of endothelial cell proliferation
          • S1P induces proliferation of VECs. [16]
          • S1P receptor-mediated signaling plays a major regulatory role in angiogenesis. [14]
        • positive regulation of blood vessel endothelial cell migration
          • S1P induces migration of VECs. [13]
          • S1P receptor-mediated signaling plays a major regulatory role in angiogenesis. [14]
          • VEC migration is inhibited by antisense oligonucleotides against s1p3. [15]
        • adherens junction assembly
          • S1P-induced VEC adherens junction assembly and cell barrier integrity are blocked by antisense oligonucleotides against s1p3. [17]
          • S1P stimulates the formation and maintenance of VECs assembly/integrity by activating S1P3. [18]

      • Receptor: 5-HT-2B

        Induced phenotype:

        • carcinoid syndrome
          • Carcinoid tumors are characterized by their production of hormonal substances such as 5-hydroxytryptamine. The pathogenesis of the cardiac lesions and the bronchoconstriction is unknown, but the former probably involves activation of serotonin 5-HT2B receptors by serotonin. [19]

      • Receptor: PPARgamma1

        • PPARγ1 has a broader expression pattern that extends to settings such as the gut, brain, vascular cell and specific kinds of immune and inflammatory cells. [20]

      • Receptor: EPHB4

        • The receptor fo ephrin-B2, Eph-B4, is expressed on venous cells. [21]

        Induced phenotype:

        • vasculogenesis
          • Recently, ephrinB2 has been shown to be required for the remodeling of the embryonic vascular system. [21]
          • Because of its exclusive expression on arteries and the complementary expression of one of its cognate receptors, EphB4, on veins, it was suggested that ephrinB2 acts both as a ligand and as a receptor for EphB4. [21]
      Reference