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Details for anatomical structure: continuous vascular endothelial cell of blood vessels and lymphatics

EndoNet ID: ENC00231

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Synonyms

continuous vascular endothelial cell of blood vessels and lymphatics, , Endotheliocytus nonfenestratus

General information

lining blood vessels and lymphatics

Links to other resources

Cytomer cy0011246

Larger structures

  • circulatory_system__hematopoietic_system
  • parts_of_human_body
  • blood_vessel
  • lung

Substructures

    Secreted hormones

    • Hormone: pentraxin 3

      • PTX3 is made by diverse cell types, most prominently endothelial cells, macrophages and dendritic cells, in response to primary inflammatory signals (e.g. interleukin-1 (IL-1), tumour necrosis factor (TNF), lipopolysaccharide (LPS)). [1]

    • Hormone: alpha-AGP

      • AGP, a highly glycosylated polypeptide chain, is expressed in human liver and in other cells, including human breast epithelial cells, endothelial cells, and cultured human granulocytes and monocytes. [2]

    • Hormone: ADM

      • Adrenomedullin is synthesized and secreted in abundance by endothelial cells. [3]

    • Hormone: ICAM-1

    • Hormone: IL-18

    • Hormone: C-C motif chemokine 2

      • Superoxide, H2O2, and iron are required for TNF-alpha-induced MCP-1 gene expression in endothelial cells. [4]
      • LPA induces expression of cytokines such as MCP-1 in vascular endothelial cells. [5]

      Influenced by:

      • Lysophosphatidic acid receptor 3
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

    • Hormone: PDGFA

      • Human endothelial cells express platelet-derived growth factor B chain. [6]

    • Hormone: PDGFB

      • Human endothelial cells express platelet-derived growth factor B chain. [6]
      • Recruitment of mesengial cells into the developing vascular tuft is dependent upon endothelial cell secretion of platelet-derived growth factor B. [7]

    • Hormone: ENA-78

    • Hormone: VCAM1 soluble form

    • Hormone: CLC

    • Hormone: GM-CSF

    • Hormone: M-CSF

    • Hormone: MCH

    • Hormone: eotaxin

      • Human eotaxin is an 8,3-kDa, 74-amino-acid residue, nonglycosylated polypeptide secreted by endothelial cells, fibroblasts, macrophages, ciliated and nonciliated bronchial epithelial cells, smooth muscle cells, chondrocytes, and eosinophils. [8]

    • Hormone: fibronectin

    • Hormone: thrombospondin 1

    • Hormone: laminin subunit gamma-1

    • Hormone: TNFSF18

    • Hormone: CTGF

    • Hormone: TIMP-4

    • Hormone: TNFSF15

    • Hormone: IL-8

      • LPA induces expression of cytokines such as IL-8 in vascular endothelial cells. [5]

      Influenced by:

      • Lysophosphatidic acid receptor 3
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

    • Hormone: soluble VEGFR-1

      • Microvascular and macrovascular endothelial cells.

    • Hormone: EGF

    • Hormone: FGF-1 isoform 1

    • Hormone: sALCAM

    • Hormone: soluble P-selectin

    • Hormone: soluble E-selectin

    • Hormone: von Willebrand factor

      Influenced by:

      • Vascular endothelial growth factor receptor 2
        in microvascularendothelial_cell
        • VEGF receptor-2 (VEGFR2), but not VEGFR1, is responsible for VEGF-induced release of von Willebrand factor (vWF), a major marker of endothelial Weibel-Palade bodies WPBs. [9]

    • Hormone: EETs

    • Hormone: lysyl-bradykinin

    • Hormone: bradykinin

    • Hormone: PGI2

    • Hormone: NO

      Influenced by:

      • angiotensin receptor 2
        in adipose_tissue
        • Activation of AT2 results in the production of NO and activation of several phosphatases, such as PTPase and PP2A, resulting in the inactivation of MAPK and changes in potassium and calcium current. [10]
      • insulin receptor
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics
        • The insulin receptor tyrosine kinase, phosphatidylinositol 3-kinase (PI 3-kinase), and Akt are essential components of insulin-signaling pathways related to production of NO in vascular endothelium [11]

    • Hormone: IL-1F5

    • Hormone: annexin A2

      Influenced by:

      • IGF-1R
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics
        • Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied by an increased amount of extracellular annexin II [12]
      • insulin receptor
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics
        • Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied by an increased amount of extracellular annexin II [12]

    • Hormone: interleukin 6

      Influenced by:

      • Vascular endothelial growth factor receptor 1
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics
        • VEGF-stimulated interleukin-6 release from endothelium is selectively mediated through VEGFR1. [9]

    • Hormone: IL-1 beta

      • LPA induces expression of cytokines such as IL-1beta in vascular endothelial cells. [5]

      Influenced by:

      • Lysophosphatidic acid receptor 3
        in continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

    • Hormone: sphingosine 1-phosphate

      • Endothelial cells that are subjected in vitro to laminar shear stress, which is a physiological stimulus, have increased production and secretion of S1P. [13]

    Receptors

    • Receptor: H1

    • Receptor: H2

    • Receptor: leptin receptor isoform b

      Influences:

      • endothelin-1
        • Leptin is able to upregulate ET-1 production in human umbilical vein endothelial cells. [14]

    • Receptor: Tie2

    • Receptor: activin receptor type I

    • Receptor: T-cadherin

    • Receptor: MC1R

    • Receptor: PPAR-gamma1

    • Receptor: thrombospondin receptor

      Induced phenotype:

      • negative regulation of angiogenesis
        • CD36 mediates the antiangiogenic signal of TSP-1. [15]

    • Receptor: PLXND1

    • Receptor: TNFRSF12A

      Induced phenotype:

      • regulation of endothelial cell migration
        • TNFSF12 regulates an endothelial cell wound closure rate via its receptor TNFRSF12 who is important for endothelial cell migration. [16]

    • Receptor: hepatocyte growth factor receptor

      Induced phenotype:

      • positive regulation of cell growth
        • In epithelial cells, plexin-B1 forms a functional receptor complex with Met (the scatter factor-1/hepatocyte growth factor receptor). [17]
        • Activation of Met through plexin-B1 requires the extracellular domains of both receptors. The phosphorylation of the plexin-B1/Met complex induced by CD100/Sema4D, which is significantly increased when both CD100/Sema4D and the Met ligand scatter factor-1 are present, is crucial for epithelial cell invasive growth. [18]

    • Receptor: TLR2

    • Receptor: TLR4

    • Receptor: TLR1

    • Receptor: TLR3

    • Receptor: TLR5

    • Receptor: ADAM17

      Induced phenotype:

      • regulation of angiogenesis
        • ADAM-17 regulates angiogenesis via its effects on the proliferation of endothelial cells, network formation, invasion and activation of MMP-2. [19]

    • Receptor: ALCAM

    • Receptor: TrpV4-A

      Induced phenotype:

      • regulation of cell communication
        • EETs are biologically important signal transduction molecules that have been implicated in numerous biological processes including communication between endothelial and vascular smooth muscle cells. [20]
        • TRPV4 has a potential role in the regulation of vascular homeostasis and in the regulation of endothelial cell signaling. [21]
        • TRPV4 is a possible epoxyeicosatrienoic acid(EET)-regulated Ca2+ entry channel in mouse aorta endothelium. [21]

    • Receptor: MRC2

    • Receptor: insulin receptor

      Influences:

      • annexin A2
        • Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied by an increased amount of extracellular annexin II [12]
      • NO
        • The insulin receptor tyrosine kinase, phosphatidylinositol 3-kinase (PI 3-kinase), and Akt are essential components of insulin-signaling pathways related to production of NO in vascular endothelium [11]

    • Receptor: IGF-1R

      Influences:

      • annexin A2
        • Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied by an increased amount of extracellular annexin II [12]

    • Receptor: Vascular endothelial growth factor receptor 1

      Induced phenotype:

      • regulation of angiogenesis
        • VEGF is a crucial regulator of angiogenesis.
      • positive regulation of endothelial cell proliferation
        • VEGF promotes proliferation, migration, and survival of endothelial cells. [22]
      • positive regulation of endothelial cell migration
        • VEGF promotes proliferation, migration, and survival of endothelial cells. [22]
      • inflammation
        • VEGF contributes to imflammation independent of its angiogenic functions. [23]

      Influences:

      • interleukin 6
        • VEGF-stimulated interleukin-6 release from endothelium is selectively mediated through VEGFR1. [9]

    • Receptor: Lysophosphatidic acid receptor 3

      Influences:

      • C-C motif chemokine 2
      • IL-1 beta
      • IL-8

    • Receptor: Integrin alpha-3

      Induced phenotype:

      • glomerulogenesis
        • Together, podocytes and endothelial cells synthesize the glomerular basement membrane (GBM) and assemble the tri-layered glomerular filtration barrier. Major GBM components, such as laminin alpha5, form a structural framework for glomerular development, and both laminin alpha5 and its receptor alpha3 integrin are required for glomerulogenesis. [24]

    • Receptor: Vascular endothelial growth factor receptor 2

      Influences:

      • VEGF-165

    • Receptor: Sphingosine 1-phosphate receptor 1

      Induced phenotype:

      • cell-cell junction organization
        • S1PR1 has an important role in strengthening endothelial-cell–endothelial-cell junctional contacts. [25]
      • vasculogenesis
        • S1PR1 has an important role in regulating endothelial-cell organization during development. [26]
      • positive regulation of endothelial cell migration
        • S1P stimulates the migration of endothelial cells. [27]
      • regulation of endothelial cell differentiation
        • S1PR1 is the receptor for the lysosphingolipid sphingosine 1-phosphate (S1P). S1P is a bioactive lysophospholipid that elicits diverse physiological effect on most types of cells and tissues. This inducible epithelial cell G-protein-coupled receptor may be involved in the processes that regulate the differentiation of endothelial cells. [28]

    • Receptor: Lysophosphatidic acid receptor 1

    • Receptor: Lysophosphatidic acid receptor 2

    • Receptor: G-protein coupled receptor 4

      Induced phenotype:

      • positive regulation of cell growth
        • A strong mitogenic effect of SPC was observed in a large number of cell types, such as endothelial cells from different vascular beds. [29]
        • Of the high-affinity SPC-GPCRs identified so far, GPR4 mediated stimulation of cell growth. [30]
    Reference