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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of epidermal growth factor receptor transactivation in endothelin-1-induced enhanced expression of Gi protein and proliferation in A10 vascular smooth muscle cells
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Role of epidermal growth factor receptor transactivation in endothelin-1-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内皮素1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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We have recently shown that vasoactive peptides such as angiotensin II (Ang II) and endothelin-1 (ET-1) increase the expression of Gi proteins and the proliferation of A10 vascular smooth muscle cells (VSMC) through mitogen-activated protein (MAP) kinase - phosphoinositide (PI) 3-kinase pathways. This study was intended to examine the implication of epidermal growth factor receptor (EGFR) activation in ET-1-induced enhanced expression of Gi proteins and proliferation of A10 VSMC, and to further investigate the underlying mechanisms responsible for these increases. Cell proliferation was determined by [3H]thymidine incorporation and the expression of Gi proteins; extracellular signal-regulated kinases 1 and 2 (ERK1/2) and EGFR phosphorylation was determined by Western blotting. Treatment of A10 VSMC with ET-1 enhanced the expression of Gi proteins, which was attenuated by BQ123 and BQ788, antagonists of ETA and ETB receptor respectively. In addition, ET-1 enhanced the phosphorylation of EGFR in A10 VSMC, which was restored to the control levels by EGFR inhibitor and ETA and ETB receptor antagonists. Furthermore, ET-1 also augmented the proliferation and ERK1/2 phosphorylation of A10 VSMC, which were restored to the control levels by inhibition of EGFR. These data suggest that ET-1 transactivates EGFR, which, through MAP kinase signaling, may contribute to the enhanced expression of Gi proteins and thus 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）通过有丝分裂原激活蛋白（MAP）来增加Gi蛋白的表达和A10血管平滑肌细胞（VSMC）的增殖。激酶-磷酸肌醇（PI）3-激酶途径。这项研究旨在检查表皮生长因子受体（EGFR）激活在ET-1诱导的Gi蛋白表达增强和A10 VSMC增殖中的意义，并进一步研究造成这些增加的潜在机制。细胞增殖通过[3 H]胸苷的掺入和Gi蛋白的表达来确定。细胞外信号调节激酶1和2（ERK1 / 2）和EGFR磷酸化通过蛋白质印迹法确定。用ET-1处理A10 VSMC可增强Gi蛋白的表达，而G蛋白则被ETA和ETB受体拮抗剂BQ123和BQ788减弱。此外，ET-1增强了A10 VSMC中EGFR的磷酸化，该水平通过EGFR抑制剂以及ETA和ETB受体拮抗剂恢复至对照水平。此外，ET-1还增强了A10 VSMC的增殖和ERK1 / 2磷酸化，可通过抑制EGFR恢复到对照水平。这些数据表明，ET-1可激活EGFR，而EGFR通过MAP激酶信号转导可能会增强Gi蛋白的表达，从而增加A10 VSMC的增殖。

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