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首页> 外文期刊>Journal of Cellular Physiology >Cytoskeletal remodeling in vascular smooth muscle cells in response to angiotensin II-induced activation of the SHP-2 tyrosine phosphatase.
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Cytoskeletal remodeling in vascular smooth muscle cells in response to angiotensin II-induced activation of the SHP-2 tyrosine phosphatase.

机译:在血管平滑肌细胞骨架重塑血管紧张素II-induced细胞反应SHP-2酪氨酸磷酸酶的激活。

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摘要

Angiotensin II is an octapeptide that regulates diverse cellular responses including the actin cytoskeletal organization. In this study, stable cell lines overexpressing wild-type or catalytically inactive SHP-2 were employed to elucidate the signaling pathway utilized by the SHP-2 tyrosine phosphatase that mediates an angiotensin II-induced reorganization of the actin cytoskeleton in vascular smooth muscle cells (VSMC). The expression of wild-type SHP-2 prevented an angiotensin II dependent increase in stress fiber formation. In contrast, the catalytically inactive mutant SHP-2 increased stress fiber formation. Additional observations further established that SHP-2 regulates the reorganization of the actin cytoskeleton through RhoA- and Vav2-dependent signaling pathways. The expression of wild-type SHP-2 caused a dephosphorylation of several focal adhesion associated proteins including paxillin, p130Cas, and tensin in VSMC. This dephosphorylation of focal adhesion associated proteins was accompanied by significantly decreased numbers of focal adhesions within cells. These results demonstrate a unique role for SHP-2 in the regulation of the cellular architecture of VSMC, suggesting the possibility that this phosphatase might be instrumental in vascular remodeling.
机译:血管紧张素ⅱ是一个八肽调节不同的细胞反应,包括肌动蛋白细胞骨架组织。细胞系overexpressing野生型或SHP-2被用来催化地无所作为阐明所利用的信号通路SHP-2酪氨酸磷酸酶调节血管紧张素II-induced重组在血管平滑肌肌动蛋白细胞骨架细胞(VSMC)。预防血管紧张素ⅱ的依赖增加应力纤维的形成。催化地不活跃的突变SHP-2增加应力纤维的形成。进一步证实SHP-2调节的肌动蛋白细胞骨架重组RhoA Vav2-dependent信号通路。野生型SHP-2引起了的表情去磷酸化的几个焦点粘连相关的蛋白质包括桩蛋白、p130Cas并在VSMC tensin。粘着斑相关蛋白质伴随着显著减少的数量焦粘连细胞内。演示SHP-2的独特作用监管VSMC的细胞结构,建议这磷酸酶的可能性可能在血管重建。

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