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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Contribution of epidermal growth factor receptor transactivation in angiotensin II-induced enhanced expression of Gi protein and proliferation in A10 vascular smooth muscle cells.
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Contribution of epidermal growth factor receptor transactivation in angiotensin II-induced enhanced expression of Gi protein and proliferation in A10 vascular smooth muscle cells.

机译：表皮生长因子受体反式激活在血管紧张素II诱导的Gi蛋白表达增强和A10血管平滑肌细胞增殖中的作用。

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摘要

We have recently shown that vasoactive peptides such as angiotensin II (Ang II) and endothelin-1 (ET-1) increased the expression of G(i) proteins and proliferation of A10 vascular smooth muscle cells (VSMC) through MAP kinase / PI3 kinase pathways. The present study was undertaken to examine the implication of growth factor receptor activation in Ang II-induced enhanced expression of G(i) proteins and proliferation of A10 VSMC and to further investigate the underlying mechanisms responsible for these increases. Cell proliferation was determined by [(3)H]thymidine incorporation, and the expression of G(i) proteins and the phosphorylation of ERK1/2 and epidermal growth factor receptor (EGFR) was determined by Western blotting. Treatment of A10 VSMC with Ang II enhanced the expression of Gi proteins, which was attenuated by Ang II AT(1) receptor antagonist but not by AT(2) receptor antagonist. The inhibitor of EGFR also attenuated the enhanced expression of G(i) proteins induced by Ang II to control levels. In addition, Ang II enhanced the phosphorylation of EGFR in A10 VSMC, and this was restored to control levels by the EGFR inhibitor and antioxidants. Furthermore, Ang II also augmented the proliferation and ERK1/2 phosphorylation of A10 VSMC, which were restored to control levels by the EGFR inhibitor. These data suggest that the Ang II-induced increase in oxidative stress transactivates EGFR, which through MAP kinase signaling may contribute to the enhanced expression of G(i) proteins and thereby to the increased proliferation of A10 VSMC.
机译：我们最近发现血管活性肽，例如血管紧张素II（Ang II）和内皮素1（ET-1）通过MAP激酶/ PI3激酶增加了G（i）蛋白的表达和A10血管平滑肌细胞（VSMC）的增殖途径。进行本研究以检查生长因子受体激活在Ang II诱导的G（i）蛋白表达增强和A10 VSMC增殖中的含义，并进一步研究造成这些增加的潜在机制。通过[（3）H]胸苷掺入确定细胞增殖，并通过Western印迹确定G（i）蛋白的表达以及ERK1 / 2和表皮生长因子受体（EGFR）的磷酸化。 Ang II处理A10 VSMC增强了Gi蛋白的表达，Ang II AT（1）受体拮抗剂减弱了该蛋白的表达，而AT（2）受体拮抗剂未减弱该蛋白的表达。 EGFR的抑制剂还减弱了由Ang II诱导的G（i）蛋白表达的增强，从而达到控制水平。此外，Ang II增强了A10 VSMC中EGFR的磷酸化，并通过EGFR抑制剂和抗氧化剂将其恢复至控制水平。此外，Ang II还增强了A10 VSMC的增殖和ERK1 / 2磷酸化，可通过EGFR抑制剂将其恢复至对照水平。这些数据表明，Ang II诱导的氧化应激增加会激活EGFR，EGFR通过MAP激酶信号传导可能有助于G（i）蛋白表达的增强，从而促进A10 VSMC的增殖。

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