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Early Response of Endothelial Cells to Flow Is Mediated by VE-Cadherin

机译:VE-钙黏着蛋白介导内皮细胞对血流的早期反应

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Endothelial cells are known to respond to flow onset by increasing actin turnover rate. Current models assume that an increase in the actin turnover rate should result in a rise in cell crawling speed. Here we report that confluent endothelial monolayer shows an unexpected behavior: cell crawling speed decreases by 40% within the first 30 min of flow onset. A drop in crawling speed has not been observed in either subconfluent endothelial cells or in VE-cadherin-deficient cells. We found that flow onset caused an increase in the number of VE-cadherin-GFP molecules in the junctions and elicited changes in the cytoskeleton-associated fractions of , -catenins and VE-cadherin. Flow application also increased the strength of interactions of endothelial cells with surfaces coated with recombinant VE-cadherin. These observations suggest that endothelial cell junctional proteins respond to flow transiently by increasing the strength of intercellular attachments early after flow onset and support the view on the active role of intercellular adhesions in mechanotransduction.
机译:已知内皮细胞通过增加肌动蛋白周转率来响应血流开始。当前模型假定肌动蛋白周转率的增加应导致细胞爬行速度的提高。在这里,我们报道了汇合的内皮单层细胞表现出意想不到的行为:在开始流动的前30分钟内,细胞爬行速度降低了40%。在汇合的内皮细胞或缺乏VE-钙粘蛋白的细胞中均未观察到爬行速度下降。我们发现,流量发作导致连接中的VE-钙粘着蛋白-GFP分子数量增加,并引起β-连环蛋白和VE-钙粘着蛋白的细胞骨架相关部分的变化。流动施加还增加了内皮细胞与用重组VE-钙粘蛋白包被的表面相互作用的强度。这些观察结果表明,内皮细胞连接蛋白在血流开始后早期通过增加细胞间附着的强度来瞬时响应血流,并支持关于细胞间粘附在机械转导中的积极作用的观点。

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