Shear stress regulates late EPC differentiation via mechanosensitive molecule-mediated cytoskeletal rearrangement.
Shear stress regulates late EPC differentiation via mechanosensitive molecule-mediated cytoskeletal rearrangement.
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剪切应力通过机械敏感分子介导的细胞骨架重排调节晚期 EPC 分化。
DOI：
10.1371/journal.pone.0067675
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Avsar E
中科院分区：
文献类型：
--
作者：
Cheng M;Guan X;Li H;Cui X;Zhang X;Li X;Jing X;Wu H;Avsar E
以往的研究表明，内皮祖细胞（EPCs），特别是晚期EPCs，在内皮细胞的维护和修复中发挥重要作用。最近的证据表明，切应力是EPC分化的关键调节因子。然而，剪切应力诱导的EPC分化的潜在机制尚未完全理解。本研究旨在进一步探讨切应力对EPC晚期分化的影响及其信号机制。在体外和体内试验表明，细胞骨架重塑参与了剪切应力上调表达的内皮标志物vWF和CD 31在晚期EPCs，随后增加在体内动脉损伤后再内皮化。此外，剪切应力激活了多种机械敏感性分子，包括整合素β1、Ras、ERK 1/2、桩蛋白和FAK，它们都参与了晚期EPCs响应剪切应力的细胞骨架重排和细胞分化。切应力是EPC向内皮细胞分化的关键调节因子，对血管修复具有重要意义，而整合素β1、Ras、ERK 1/2、桩蛋白和FAK级联反应介导的细胞骨架重排在这一过程中起着至关重要的作用。
Previous studies have demonstrated that endothelial progenitor cells (EPCs), in particular late EPCs, play important roles in endothelial maintenance and repair. Recent evidence has revealed shear stress as a key regulator for EPC differentiation. However, the underlying mechanisms regulating the shear stress–induced EPC differentiation have not been understood completely. The present study was undertaken to further investigate the effects of shear stress on the late EPC differentiation, and to elucidate the signal mechanism involved. In vitro and in vivo assays revealed that cytoskeletal remodeling was involved in the shear stress-upregulated expression of endothelial markers vWF and CD31 in late EPCs, with subsequently increased in vivo reendothelialization after arterial injury. Moreover, shear stress activated several mechanosensitive molecules including integrin β1, Ras, ERK1/2, paxillin and FAK, which were all involved in both cytoskeletal rearrangement and cell differentiation in response to shear stress in late EPCs. Shear stress is a key regulator for late EPC differentiation into endothelial cells, which is important for vascular repair, and the cytoskeletal rearrangement mediated by the activation of the cascade of integrin β1, Ras, ERK1/2, paxillin and FAK is crucial in this process.
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影响因子：
4.8
作者：
Shepherd, Benjamin R.;Enis, David R.;Schechner, Jeffrey S.
通讯作者：
Schechner, Jeffrey S.
影响因子：
4.8
作者：
Tanaka, Kimie;Sata, Masataka;Nagai, Ryozo
通讯作者：
Nagai, Ryozo
影响因子：
20.1
作者：
Schroeter, Marco R.;Leifheit, Maren;Schaefer, Katrin
通讯作者：
Schaefer, Katrin
影响因子：
11.4
作者：
Tzima, E;del Pozo, MA;Schwartz, MA
通讯作者：
Schwartz, MA
DOI：
10.1152/ajpheart.00519.2004
发表时间：
2005-02-01
影响因子：
4.8
作者：
Radel, C;Rizzo, V
通讯作者：
Rizzo, V