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首页> 外文期刊>American Journal of Physiology >ERK activation and mitogenesis in human airway smooth muscle cells.
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ERK activation and mitogenesis in human airway smooth muscle cells.

机译：人气道平滑肌细胞中的ERK活化和有丝分裂。

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摘要

Asthmatic airways are characterized by an increase in smooth muscle mass, due mainly to hyperplasia. Many studies suggest that extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2, respectively), one group of the mitogen-activated protein (MAP) kinase superfamily, play a key role in the signal transduction pathway leading to cell proliferation. PGE(2) and forskolin inhibited mitogen-induced ERK activation. Inhibition of MAP kinase kinases 1 and 2 (MEK1 and MEK2, respectively), which are upstream from ERK, with the specific MEK inhibitor U-0126 blocked both cell proliferation and ERK activation. In addition, U-0126 inhibited mitogen-induced activation of p90 ribosomal S6 kinase and expression of c-Fos and cyclin D1, all of which are downstream from ERK in the signaling cascade that leads to cell proliferation. Antisense oligodeoxynucleotides directed to ERK1 and -2 mRNAs reduced ERK protein and cell proliferation. These results indicate that ERK is required for human airway smooth muscle cell proliferation. Thus targeting the control of ERK activation may provide a new therapeutic approach for hyperplasia seen in asthma.
机译：哮喘气道的特征是平滑肌质量增加，这主要是由于增生引起的。许多研究表明，细胞外信号调节激酶1和2（分别为ERK1和ERK2）是一组有丝分裂原激活蛋白（MAP）激酶超家族，在导致细胞增殖的信号转导途径中起关键作用。 PGE（2）和福司可林抑制有丝分裂原诱导的ERK激活。用特定的MEK抑制剂U-0126抑制ERK上游的MAP激酶激酶1和2（分别为MEK1和MEK2）可同时阻止细胞增殖和ERK活化。此外，U-0126抑制了有丝分裂原诱导的p90核糖体S6激酶的活化以及c-Fos和cyclin D1的表达，所有这些都位于导致细胞增殖的信号级联反应中ERK的下游。直接针对ERK1和-2 mRNA的反义寡脱氧核苷酸可降低ERK蛋白和细胞增殖。这些结果表明ERK是人气道平滑肌细胞增殖所必需的。因此，靶向控制ERK激活可为哮喘中出现的增生提供一种新的治疗方法。

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