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首页> 外文期刊>Journal of Cellular Physiology >Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion-associated proteins.
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Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion-associated proteins.

机译：剪切应力调节内皮细胞形态通过监管和f -肌动蛋白组织焦adhesion-associated蛋白质。

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Flow-related shear stress has been shown to modulate endothelial cell structure and function including F-actin microfilament organization. Focal adhesion-associated proteins such as vinculin, talin, and specific integrins may play a role in the modulation of these cytoskeletal and morphological changes. Double-label immunofluorescence studies indicated that, in static culture, alpha 5 beta 1 fibronectin receptors (alpha 5 beta 1 FNRs) and alpha v beta 3 vitronectin receptors (alpha v beta 3 VNRs) were found predominantly in the peripheral regions of bovine aortic endothelial cells (BAECs) corresponding to the localization of vinculin, talin, and actin microfilament terminations. In response to shear stress, concomitant with cell elongation and the appearance of stress fibers aligned with the direction of flow, there was a prominent localization of vinculin and alpha v beta 3 VNRs as the "upstream" end of the cells. Stress fiber terminations were clearly evident at these concentrations of focal adhesion-associated proteins. These data suggest that the upstream concentration of these proteins may direct shear stress-induced stress fiber formation and may function in the alignment of the fibers in the direction of flow. Levels of surface alpha v beta 3 VNRs were found to decrease in response to flow, possibly reflecting the decrease in numbers of "downstream" receptors. Unlike the arrangement of vinculin and alpha v beta 3 VNRs observed following exposure to flow, talin and alpha 5 beta 1 FNRs, in addition to being localized at the upstream end of the cell, were also evenly distributed throughout the rest of the cell. Surface levels of alpha 5 beta 1 FNRs increased in response to shear stress, perhaps providing an increased adherence of BAECs to the extracellular matrix through these receptors. These data suggest that focal adhesion-associated proteins play specific roles in the response of BAECs to shear stress.
机译：从流量剪切应力已被证明调节内皮细胞的结构和功能包括f -肌动蛋白微丝的组织。焦adhesion-associated蛋白质等vinculin,美丽的,和特殊的整合蛋白这些细胞骨架的调制作用和形态学变化。免疫荧光的研究表明,在静态文化、α5β1纤连蛋白(α5β1受体FNRs)β和αv3 vitronectin受体(αvβ3 VNRs)主要被发现在外围地区牛主动脉内皮细胞(BAECs)对应的本地化vinculin、蛋白和肌动蛋白微丝终止妊娠。相伴与细胞伸长的纤维与压力流的方向,突出的本地化vinculin v和αβ3 VNRs“上游”的细胞。在这些终端显然是明显焦adhesion-associated浓度蛋白质。这些蛋白质的浓度可能直接剪切压力引起的应力纤维形成和可能功能纤维的排列在一条直线上流的方向。3 VNRs被发现反应减少流,可能反映出数量减少“下游”的受体。vinculin和αvβ3 VNRs观察接触流程后,蛋白和α5β1 FNRs,除了本地化最上游的细胞,也均匀分布在整个细胞。表面FNRsα5β1的含量也增加了剪切应力,可能提供一个增加BAECs到细胞外的依从性通过这些受体矩阵。表明,焦adhesion-associated蛋白质BAECs的反应中扮演特定的角色剪切应力。

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