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首页> 外文期刊>American Journal of Physiology >ET-1 stimulates ERK signaling pathway through sequential activation of PKC and Src in rat myometrial cells.
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ET-1 stimulates ERK signaling pathway through sequential activation of PKC and Src in rat myometrial cells.

机译：ET-1通过连续激活大鼠子宫肌层细胞中的PKC和Src来刺激ERK信号通路。

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In this study, we analyzed in rat myometrial cells the signaling pathways involved in the endothelin (ET)-1-induced extracellular signal-regulated kinase (ERK) activation required for the induction of DNA synthesis. We found that inhibition of protein kinase C (PKC) by Ro-31-8220 abolished ERK activation. Inhibition of phospholipase C (PLC) by U-73122 or of phosphoinositide (PI) 3-kinase by wortmannin partially reduced ERK activation. A similar partial inhibition was observed after treatment with pertussis toxin or PKC downregulation by phorbol ester treatment. The effect of wortmannin was additive with that produced by PKC downregulation but not with that due to pertussis toxin. These results suggest that both diacylglycerol-sensitive PKC, activated by PLC products, and diacylglycerol-insensitive PKC, possibly activated by a G(i)-PI 3-kinase-dependent process, are involved in ET-1-induced ERK activation. These two pathways were found to be activated mainly through the ET(A) receptor subtype. ET-1 and phorbol ester stimulated Src activity in a PKC-dependent manner, both responses being abolished in the presence of Ro-31-8220. Inhibition of Src kinases by PP1 abrogated phorbol ester- and ET-1-induced ERK activation. Finally, ET-1 activated Ras in a PP1- and Ro-31-8220-sensitive manner. Altogether, our results indicate that ET-1 induces ERK activation in rat myometrial cells through the sequential stimulation of PKC, Src, and Ras.
机译：在这项研究中，我们分析了大鼠子宫肌层细胞中涉及内皮素（ET）-1诱导的细胞外信号调节激酶（ERK）激活所涉及的信号传导途径，这些活化是DNA合成的诱导所必需的。我们发现Ro-31-8220对蛋白激酶C（PKC）的抑制作用消除了ERK激活。 U-73122抑制磷脂酶C（PLC）或渥曼青霉素抑制磷脂酰肌醇（PI）3-激酶可部分降低ERK活化。用佛波酯处理百日咳毒素或PKC下调后，观察到类似的部分抑制。渥曼青霉素的作用与PKC下调产生的作用相加，但与百日咳毒素无关。这些结果表明，由PLC产品激活的对二酰基甘油敏感的PKC和可能由G（i）-PI 3-激酶依赖性过程激活的对二酰基甘油不敏感的PKC都参与了ET-1诱导的ERK激活。发现这两个途径主要通过ET（A）受体亚型激活。 ET-1和佛波酯以PKC依赖的方式刺激Src活性，在Ro-31-8220的存在下，两种反应均被取消。 PP1对Src激酶的抑制作用消除了佛波酯和ET-1诱导的ERK活化。最后，ET-1以对PP1和Ro-31-8220敏感的方式激活了Ras。总之，我们的结果表明，ET-1通过依次刺激PKC，Src和Ras诱导大鼠子宫肌层细胞中的ERK活化。

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