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首页> 外文期刊>American Journal of Physiology >Endothelial actin cytoskeleton remodeling during mechanostimulation with fluid shear stress.
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Endothelial actin cytoskeleton remodeling during mechanostimulation with fluid shear stress.

机译：流体剪切应力的机械刺激过程中内皮肌动蛋白的细胞骨架重塑。

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Fluid shear stress stimulation induces endothelial cells to elongate and align in the direction of applied flow. Using the complementary techniques of photoactivation of fluorescence and fluorescence recovery after photobleaching, we have characterized endothelial actin cytoskeleton dynamics during the alignment process in response to steady laminar fluid flow and have correlated these results to motility. Alignment requires 24 h of exposure to fluid flow, but the cells respond within minutes to flow and diminish their movement by 50%. Although movement slows, the actin filament turnover rate increases threefold and the percentage of total actin in the polymerized state decreases by 34%, accelerating actin filament remodeling in individual cells within a confluent endothelial monolayer subjected to flow to levels used by dispersed nonconfluent cells under static conditions for rapid movement. Temporally, the rapid decrease in filamentous actin shortly after flow stimulation is preceded by an increase in actin filament turnover, revealing that the earliest phase of the actin cytoskeletal response to shear stress is net cytoskeletal depolymerization. However, unlike static cells, in which cell motility correlates positively with the rate of filament turnover and negatively with the amount polymerized actin, the decoupling of enhanced motility from enhanced actin dynamics after shear stress stimulation supports the notion that actin remodeling under these conditions favors cytoskeletal remodeling for shape change over locomotion. Hours later, motility returned to pre-shear stress levels but actin remodeling remained highly dynamic in many cells after alignment, suggesting continual cell shape optimization. We conclude that shear stress initiates a cytoplasmic actin-remodeling response that is used for endothelial cell shape change instead of bulk cell translocation.
机译：流体剪切应力刺激诱导内皮细胞在施加的流动方向上伸长和排列。使用互补的光活化荧光和光漂白后的荧光恢复的互补技术，我们表征了对齐过程中内皮肌动蛋白细胞骨架的动力学特性，以响应稳定的层状液流并将这些结果与运动性相关联。对准需要暴露于液流中24小时，但是细胞会在数分钟内响应液流并将其运动减少50％。尽管运动变慢，但肌动蛋白丝的周转率增加了三倍，聚合状态下总肌动蛋白的百分比降低了34％，加速了融合内皮单层内单个细胞中肌动蛋白丝的重塑，使其在静态下流动至分散的非融合细胞所使用的水平快速运动的条件。暂时地，在流动刺激后不久，丝状肌动蛋白的迅速减少之前是肌动蛋白丝周转的增加，这表明肌动蛋白细胞骨架对剪切应力的最早反应是净细胞骨架解聚。但是，与静态细胞不同，在静态细胞中，细胞运动性与细丝周转率呈正相关，而与聚合的肌动蛋白呈负相关，在剪切应力刺激后，增强的运动性与增强的肌动蛋白动力学脱钩，支持了在这些条件下肌动蛋白重塑有利于细胞骨架的观点。重塑运动形状。数小时后，运动性恢复到剪切前的应力水平，但肌动蛋白重塑在对齐后在许多细胞中仍然保持高度动态，这表明细胞形状一直在不断优化。我们得出的结论是，剪应力会启动细胞质肌动蛋白重塑反应，该反应可用于内皮细胞形状改变而不是大细胞转运。

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