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      Medial and Endothelial Platelet-Derived Growth Factor A Chain Expression Is Regulated by in vivo Exposure to Elevated Flow

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          Previous work from this laboratory demonstrated that in vivo exposure to elevated arterial flow stimulates endothelial and smooth muscle cell hyperplasia concomitant with lumen enlargement, medial wall hypertrophy, and increases in medial extracellular connective tissue in rat mesenteric small arteries. In an effort to elucidate the role of growth factors in mediating this arterial remodeling response, in situ hybridization was performed on control and high flow arterial sections using <sup>35</sup>S-labeled riboprobes for PDGF-A, PDGF-B, basic FGF, and TGFβ<sub>1</sub> mRNA. Results demonstrate that after exposure to elevated arterial flow for 24 h, expression of PDGF-A mRNA in the media was significantly elevated over basal levels (+215%, p < 0.001). This expression decreased towards control levels by 3 and 7 days. Increased endothelial expression of PDGF-A mRNA over basal levels was evident after 3 and 7 days of elevated flow (+129%, p < 0.01; +182%; p < 0.01, respectively). Acute medial PDGF-A mRNA expression may result from elevated circumferential hoop stress secondary to flow-induced dilation while delayed expression in the endothelium may result from normalization of wall shear stress. Endothelial expression of PDGF-B mRNA was significantly elevated over control levels (+62%, p < 0.01) after exposure to high flow for 7 days. Expression of bFGF and TGFβ<sub>1</sub> mRNA was not significantly different between control and high flow vessels at all times measured. These results suggest a role for PDGF-A in regulating acute arterial remodeling following in vivo exposure to elevated flow.

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          Most cited references 2

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          Mechanical strain induces growth of vascular smooth muscle cells via autocrine action of PDGF

           Q.-A. Mai,  HE Ives,  K Sudhir (1993)
          The effect of cyclic mechanical strain on growth of neonatal rat vascular smooth muscle (VSM) cells were examined. Cells were grown on silicone elastomer plates subjected to cyclic strain (60 cycle/min) by application of a vacuum under the plates. A 48 h exposure to mechanical strain increased the basal rate of thymidine incorporation by threefold and increased cell number by 40% compared with cells grown on stationary rubber plates. Strain also increased the rate of thymidine incorporation in response to alpha-thrombin (from 15- to 33-fold), but not to PDGF. As determined by thymidine autoradiography, strain alone induced a fourfold increase in labeled nuclei at the periphery of dishes, where strain is maximal, and a 2-3-fold increase at the center of dishes. Strain appeared to induce the production of an autocrine growth factor(s), since conditioned medium from cells subjected to strain induced a fourfold increase in DNA synthesis in control cells. Western blots of medium conditioned on the cells subjected to strain indicate that the cells secrete both AA and BB forms of PDGF in response to strain. Northern blots of total cell RNA from cells exposed to strain for 24 h show increased steady-state level of mRNA for PDGF- A. Lastly, polyclonal antibodies to the AA form of PDGF reduced by 75% the mitogenic effect of strain and polyclonal antibodies to AB-PDGF reduced mitogenicity by 50%. Antibodies to bFGF did not significantly reduce the strain-induced thymidine incorporation. Thus, the mechanism of strain-induced growth appears to involve the intermediary action of secreted PDGF.
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            • Abstract: not found
            • Article: not found

            Stimulation of Transcription Factors NFκB and AP1 in Endothelial Cells Subjected to Shear Stress


              Author and article information

              J Vasc Res
              Journal of Vascular Research
              S. Karger AG
              December 1998
              23 September 2008
              : 35
              : 6
              : 413-420
              Department of Physiology, Eastern Virginia Medical School, Norfolk, Va., USA
              25612 J Vasc Res 1998;35:413–420
              © 1998 S. Karger AG, Basel

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              Page count
              Figures: 6, References: 34, Pages: 8
              Research Paper


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