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首页> 外文期刊>Cell cycle >Overexpression of caveolin-1 inhibits endothelial cell proliferation by arresting the cell cycle at G0/G1 phase.
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Overexpression of caveolin-1 inhibits endothelial cell proliferation by arresting the cell cycle at G0/G1 phase.

机译：Caveolin-1的过表达通过将细胞周期停在G0 / G1期来抑制内皮细胞增殖。

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摘要

Angiogenesis, the development of new blood vessels from preexisting capillary, is required for tumor growth and metastasis. The process is not fully understood yet, but involves endothelial cell proliferation, migration and differentiation. Recently, we have shown that overexpression of caveolin-1, a putative transformation suppressor gene, inhibits VEGFR-2 and MEK-1-mediated mitogenic signal to the nucleus. Conversely, angiogenic activators suppress caveolin-1 expression in endothelial cells. However, whether caveolin-1 expression affects endothelial cell proliferation is not clear. In the present study, we infect human endothelial cells with adenovirus expressing caveolin-1 and show that transient overexpression of caveolin-1 dramatically inhibits the proliferation of human endothelial cells. Consistent with caveolin-1 functioning as an inhibitor for protein kinases, overexpression of caveolin-1 inhibits the activity of VEGFR-2 (KDR) and down-stream p42/44 MAP kinase. Furthermore, overexpression of caveolin-1 prevents VEGF-induced down-regulation of the cyclin-dependent kinase inhibitor p27(kip1) and Rb phosphorylation, and subsequently arrests endothelial cells in the G(0)/G(1) phase. Thus, our results suggest that caveolin-1, as a negative regulator of endothelial cell proliferation, may be a potential target for the control of angiogenesis.
机译：肿瘤的生长和转移需要血管生成，即从预先存在的毛细管中产生新血管。该过程尚未完全理解，但涉及内皮细胞增殖，迁移和分化。最近，我们已经表明，caveolin-1（一种可能的转化抑制基因）的过表达抑制了VEGFR-2和MEK-1介导的细胞核有丝分裂信号。相反，血管生成激活剂抑制内皮细胞中小窝蛋白1的表达。但是，caveolin-1表达是否影响内皮细胞增殖尚不清楚。在本研究中，我们用表达caveolin-1的腺病毒感染人内皮细胞，并显示caveolin-1的瞬时过表达显着抑制了人内皮细胞的增殖。与caveolin-1起到蛋白激酶抑制剂的作用一致，caveolin-1的过表达抑制了VEGFR-2（KDR）和下游p42 / 44 MAP激酶的活性。此外，caveolin-1的过表达可防止VEGF诱导的细胞周期蛋白依赖性激酶抑制剂p27（kip1）和Rb磷酸化的下调，并随后使内皮细胞停滞在G（0）/ G（1）期。因此，我们的结果表明，caveolin-1作为内皮细胞增殖的负调节剂，可能是控制血管生成的潜在靶标。

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