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      Morphogenic Effects of Endothelin-1 on Vascular Smooth Muscle Cells

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          Endothelin-1 (ET-1), a vasoconstrictor peptide produced by endothelial and vascular smooth muscle cells (VSMC) might play a role in vascular remodelling. To investigate the proposed ‘mitogenic’ potential of ET-1, we examined the effects of chronic exposure of VSMC to ET-1 on cell cycle, growth/proliferation and differentiation under essentially mitogen-free culture conditions. Bulk cultures of thoracic aortic VSMC of spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats, although exhibiting genetically determined differences in growth/proliferation (due to shortened Gl and G2 phases in SHR VSMC), respond in a similar manner to ET-1 exposure: long-term exposure (12-15 days) of VSMC from both sources to ET-1 in nonmitogenic medium did not promote cycling of cells. On the contrary, ET-1 attenuated the cycling of VSMC which had already cycled beyond the S phase. For cells which had not cycled beyond the S phase, ET-1 interrupted progression through the cell cycle at the late Gl/early S phase. The specific ability of SHR VSMC to grow in mitogen-free medium was abolished by ET-1 most likely via down-regulation of platelet-derived growth factor (PDGF)-α receptors. Subsequent to ET-1 exposure, VSMC expressed increased levels of mRNA and protein for smooth-muscle-specific α-actin. However, expression of smooth muscle α-actin did not predominate over β-actin as observed for adult contractile VSMC in vivo. The ET-1-induced expression of smooth-muscle-specific α-actin mRNA was dose dependent (EC<sub>50</sub> approx. 2 × 10<sup>-9</sup> M), and α-actin protein expressed was associated with organized actin fibers.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 30
          : 4
          : 192-201
          Department of Research, University Hospital, Basel, Switzerland
          158994 J Vasc Res 1993;30:192–201
          © 1993 S. Karger AG, Basel

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          Pages: 10
          Research Paper


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