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首页> 外文期刊>Journal of cellular biochemistry. >Mechanism of down-regulation of L-type Ca(2+) channel in the proliferating smooth muscle cells of rat aorta.
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Mechanism of down-regulation of L-type Ca(2+) channel in the proliferating smooth muscle cells of rat aorta.

机译:下调大鼠主动脉增生的平滑肌细胞中L型Ca(2+)通道的机制。

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摘要

The mechanism of down-regulation of L-type Ca(2+) channel (L-VOC) was investigated in rat aortic smooth muscle cells in primary culture. On culture days 3-5, the cells actively incorporated the 5-bromo-2'-deoxy-uridine (BrdU), and did not respond to K(+) depolarization nor express alpha(1C) subunit of L-VOC. At confluence on day 8, BrdU incorporation decreased, and the cells up-regulated alpha(1C) subunit mRNA, expressed alpha(1C) subunit protein at cell periphery, and responded to K(+) depolarization. Treating the proliferating cells on day 3 with serum-free media or 10 microM PD98059, a MAP kinase kinase inhibitor, for 2 days induced the expression of alpha(1C) subunit protein and the responsiveness to K(+) depolarization. However, the serum starvation, but not PD98059, decreased the BrdU incorporation and increased the alpha(1C) subunit mRNA. It is concluded that the expression of L-VOC is substantially suppressed in the proliferating cells due to two mechanisms; a MAP kinase-mediated post-transcriptional down-regulation and the transcriptional down-regulation by additional mitogenic signals.
机译:在原代培养的大鼠主动脉平滑肌细胞中研究了L型Ca(2+)通道(L-VOC)下调的机制。在第3-5天的培养中,细胞主动掺入5-溴-2'-脱氧尿苷(BrdU),并且不响应K(+)去极化,也不表达L-VOC的alpha(1C)亚基。在第8天汇合时,BrdU掺入减少,细胞上调alpha(1C)亚基mRNA,在细胞外围表达alpha(1C)亚基蛋白,并对K(+)去极化产生反应。在第3天用无血清培养基或10 microM PD98059(一种MAP激酶激酶抑制剂)处理增殖细胞2天,诱导了alpha(1C)亚基蛋白的表达和对K(+)去极化的反应。但是,血清饥饿,但不是PD98059,减少了BrdU掺入并增加了alpha(1C)亚基mRNA。结论是,由于两种机制,L-VOC的表达在增殖细胞中被显着抑制。 MAP激酶介导的转录后下调和其他有丝分裂信号的转录下调。

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