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首页> 外文期刊>Journal of Cellular Physiology >Caveolin-1 and integrin beta1 regulate embryonic stem cell proliferation via p38 MAPK and FAK in high glucose.
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Caveolin-1 and integrin beta1 regulate embryonic stem cell proliferation via p38 MAPK and FAK in high glucose.

机译：Caveolin-1和整合素beta1调节胚胎通过p38 MAPK和FAK在干细胞增殖高葡萄糖。

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摘要

The involvement of caveolin-1 (Cav-1) and integrin beta1 (IN beta1) in regulation of embryonic stem (ES) cell growth by high glucose is by no means clear cut. Therefore, the aim of this study was to examine the influence of high glucose on Cav-1 and IN beta1 expression in mouse ES cells and their signaling pathways to modulate proliferation. High glucose significantly increased Cav-1 and IN beta1 expression. In addition, increased IN beta1 expression was inhibited by Cav-1 small interfering RNA (siRNA). High glucose caused reactive oxygen species generation and p38 mitogen-activated protein kinase (MAPK) phosphorylation. Inhibition of p38 MAPK blocked high glucose-induced Cav-1 and fibronectin (FN) expression. Moreover, phosphorylation of both Src and focal adhesion kinase (FAK) were increased by high glucose, which were inhibited by IN beta1 antibody. In addition, high glucose increased the expression levels of PINCH1/2, integrin-linked kinase (ILK), and alpha-parvin [PIP] complex proteins, which were all inhibited by the FAK siRNA and Src specific inhibitor (PP2, 10(-7) M). High glucose also increased F-actin expression, which was inhibited by ILK, PINCH1/2, and alpha-parvin siRNAs. Finally, high glucose-induced increase of ES cell proliferation was inhibited by TRIO and F-actin binding protein (TRIOBP) siRNA. The results demonstrate that high glucose-induced Cav-1 and IN beta1 activation can stimulate ES cell proliferation through the modification of focal adhesion signaling pathways.
机译：的参与caveolin-1 (Cav-1)和整合素beta1 (beta1)胚胎干细胞的调控(ES)细胞生长的高葡萄糖决不是明确。检查Cav-1高葡萄糖的影响和在小鼠ES细胞和beta1表达式他们的信号通路调节扩散。增加Cav-1 beta1表达式。另外,增加beta1表达式抑制由Cav-1小核RNA)。高葡萄糖活性氧引起的生成和p38增殖作用激酶磷酸化(MAPK)。MAPK阻塞高glucose-induced Cav-1和纤连蛋白(FN)表达式。磷酸化的Src和粘着斑高葡萄糖激酶(FAK)增加了,由在beta1抑制抗体。高葡萄糖,增加了表达式水平的PINCH1/2, integrin-linked激酶(亲属),和alpha-parvin (PIP)复杂的蛋白质,都被FAK siRNA和Src特定抑制剂(PP2 10(7)米),高葡萄糖也增加了f -肌动蛋白的表达,这是被同类,PINCH1/2 alpha-parvinsiRNAs。ES细胞增殖抑制了三人f -肌动蛋白结合蛋白(TRIOBP)核。结果表明,高glucose-inducedCav-1 beta1激活可以刺激ES通过修改细胞增殖粘着斑信号通路。

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