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Details for anatomical structure: smooth muscle cell

EndoNet ID: ENC00152

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Synonyms

smooth muscle cell, myocyte (smooth), Myocytus nonstriatus

Links to other resources

Cytomer cy0011297

Larger structures

    Substructures

      Secreted hormones

      • Hormone: VEGF-165

        • VEGF is produced by cultured vascular smooth muscle cells. [1]
      • Hormone: IL-18

        • Angiotensin II enhances interleukin-18 mediated inflammatory gene expression in vascular smooth muscle cells. [2]
      • Hormone: osteonectin

      • Hormone: FGF-2

      • Hormone: vasorin

      • Hormone: interleukin 6

        • Protein kinase C-mediated p38 mitogen activated protein kinase (MAPK) is responsible for IL-6 secretion. [3]
        • p38α is specifically responsible for LPA-induced IL-6 secretion. [3]

      Receptors

      • Receptor: PPARgamma1

        • PPARγ is expressed in endothelium and smooth muscle in the blood vessel wall [4]
      • Receptor: TNFRSF12A

        Induced phenotype:

        • positive regulation of smooth muscle proliferation
          • TNFSF12 induces proliferation of human aortic smooth muscle cells in vitro and acts as a potent inducer of angiogenesis. [5]
      • Receptor: vasorin

        • Vasorinis predominantly expressed by vascular smooth muscle cells. [6]

        Induced phenotype:

        • negative regulation of transforming growth factor beta receptor signaling pathway
          • Vasorin is predominantly expressed in VSMCs and modulates the vascular response to injury, at least in part, by attenuating TGF-β signaling in vivo. [6]

        Influences:

        • TGF-beta 1
          • We found that vasorin directly binds to transforming growth factor (TGF)-β and attenuates TGF-β signaling in vitro. [6]
      • Receptor: Integrin alpha-3

      • Receptor: PRLR

        Induced phenotype:

        • positive regulation of smooth muscle proliferation
          • Prolactin induces proliferation of vascular smooth muscle cells through a protein kinase C-dependent mechanism. [7]
      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • positive regulation of smooth muscle cell migration
          • Overexpression of S1PR1 in VSMCs enhances migration response to S1P. [8]
        • heart development
          • Direct evidence for S1P receptor signaling in angiogenesis and cardiovascular development comes from the phenotype of genetic-null studies in mice. The s1p1-null embryos die in utero because of defective vascular maturation in which VSMCs/pericytes do not migrate to surround the vessels. [9]
        • positive regulation of angiogenesis
          • S1P receptor edg-1 is essential for cardiovascular development. [9]
          • Edg-1 is the first G protein-coupled receptor required for blood vessel formation. In general, sphingolipid signaling is essential during mammalian development. [9]
        • regulation of inflammatory response
          • In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression. [10]
          • a central role for S1P1 in vascular smooth muscle cell migration was established by the phenotype of S1P1-deficient mice in which those cells do not migrate properly to surround and reinforce nascent vessels. [11]
      • Receptor: Lysophosphatidic acid receptor 1

        Induced phenotype:

        • negative regulation of smooth muscle cell migration
          • LPA1 and LPA2 were found to exhibit opposing effects on primary VSMCs derived from knockout mice. The migration of SMCs was increased in Lpar1−/− mice but attenuated in Lpar1−/−/Lpar2−/− mice, thus identifying LPA1 and LPA2 as negative and positive chemotactic mediators, respectively. [12]
          • LPA induces the proliferation and migration of vascular smooth muscle cells (VSMCs). [13]
        • smooth muscle cell dedifferentiation
          • Lysophosphatidic acid influences vascular cell functions, including smooth muscle cell de-differentiation. [14]
        • smooth muscle cell migration
          • Lysophosphatidic acid influences vascular cell functions, including smooth muscle cell migration. [14]
        • regulation of vascular smooth muscle cell proliferation
          • Lysophosphatidic acid influences vascular cell functions, including smooth muscle cell proliferation. [14]
        • positive regulation of smooth muscle proliferation
          • Overexpression of S1PR1 in VSMCs enhances mitogenic responses to S1P. [8]
      • Receptor: Sphingosine 1-phosphate receptor 3

        Induced phenotype:

        • vasoconstriction
          • S1P induces the vasoconstriction of isolated canine cerebral arteries via S1P receptor 3. [15]
        • regulation of inflammatory response
          • In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression. [10]
      • Receptor: Sphingosine 1-phosphate receptor 2

        Induced phenotype:

        • positive regulation of cell proliferation
          • S1P induces contraction and proliferation of smooth muscle cells. [16]
      • 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 vascular smooth muscle cells. [17]
          • Of the high-affinity SPC-GPCRs identified so far, GPR4 mediated stimulation of cell growth. [18]
      • Receptor: 5-HT-2A

        Induced phenotype:

        • vasoconstriction
          • The 5-HT 2A receptors occur peripherally on vascular smooth muscle tissue and their function is vaso-constriction. [19]
      • Receptor: integrin alpha-3/beta-1

        Induced phenotype:

        • smooth muscle cell migration
          • Binding extracellular maspin to the beta-Subunit of integrins inhibit the vascular smooth muscle migration. [20]
      • Receptor: Lysophosphatidic acid receptor 2

        Induced phenotype:

        • positive regulation of smooth muscle cell migration
          • LPA induces the proliferation and migration of vascular smooth muscle cells (VSMCs). [13]
          • LPA1 and LPA2 were found to exhibit opposing effects on primary VSMCs derived from knockout mice. The migration of SMCs was increased in Lpar1−/− mice but attenuated in Lpar1−/−/Lpar2−/− mice, thus identifying LPA1 and LPA2 as negative and positive chemotactic mediators, respectively. [12]
      • Receptor: NPR1

        • In cultured cells, NPR-A is readily found in primary vascular smooth muscle cells. [21]

        Induced phenotype:

        • vascular relaxation
          • The ability of the cardiac natriuretic peptides to relax precontracted aortic rings requires NPR-A. [21]
          • ANP stimulation of NPR-A increases intracellular cGMP concentrations which leads after several steps to vascular smooth muscle relaxation. [21]
      • Receptor: NPR2

        • NPR-B is present in aortic vascular smooth muscle . [21]

        Induced phenotype:

        • vascular relaxation
          • NPR-B is present in aortic vascular smooth muscle and mediates CNP relaxation of precontracted rat aorta. [21]
      Reference