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首页> 外文期刊>Cellular and Molecular Bioengineering >Role of Intercellular Junctions in Redistribution of Focal Adhesions and Orientation of Vascular Endothelial Cells Exposed to Cyclic Stretching
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Role of Intercellular Junctions in Redistribution of Focal Adhesions and Orientation of Vascular Endothelial Cells Exposed to Cyclic Stretching

机译：细胞间连接在局灶性粘连和循环拉伸血管内皮细胞定向中的作用。

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摘要

The redistribution of focal adhesions (FAs) containing integrin β1 and paxillin plays an important role in the cyclic stretching-induced morphological changes of endothelial cells (ECs). In addition to focal adhesion kinase (FAK), known to be a primary regulator for FA redistribution, intercellular junctions (IJs) have recently been reported to be involved in signaling upstream of FAs. Here, we addressed the role of IJs in the morphological changes and redistribution of FAs in ECs exposed to cyclic stretching. Both confluent and sparse ECs were oriented nearly perpendicularly to the stretch direction after 10 min of exposure. Orientation of sparse ECs, but not confluent ECs, was suppressed by treatment with a phospho-FAK inhibitor. FAK inhibitor blocked integrin β1 redistribution in ECs, which was observed in non-inhibited cells after 10-min stretch exposure. However, paxillin redistribution in confluent ECs was observed regardless of FAK inhibitor treatment after 2-min stretch exposure. When we blocked signals from IJs with an inhibitor of Src homology 2 domain-containing tyrosine phosphatase-2, the percentage of oriented ECs decreased and paxillin redistribution, but not integrin β1, was suppressed. These findings suggest that IJs are involved in the orientation of ECs subjected to cyclic stretching through signaling pathways other than FAK.
机译：包含整联蛋白β1和paxillin的粘着斑（FA）的重新分布在周期性拉伸诱导的内皮细胞（EC）形态变化中起重要作用。除了已知是FA重新分布的主要调节剂的粘着斑激酶（FAK）之外，最近还报道了细胞间连接（IJ）参与了FAs上游的信号传导。在这里，我们解决了IJ在暴露于循环拉伸的EC中FAs的形态变化和再分布中的作用。暴露10分钟后，融合EC和稀疏EC都几乎垂直于拉伸方向定向。稀疏EC的方向，而不是融合EC的方向，通过使用磷酸化FAK抑制剂进行了抑制。 FAK抑制剂可阻断EC中整联蛋白β1的重新分布，这是在10分钟的拉伸暴露后未抑制的细胞中观察到的。但是，在暴露2分钟后，无论FAK抑制剂如何处理，都观察到了融合EC中的Paxillin重新分布。当我们用含有Src同源性2结构域的酪氨酸磷酸酶2的抑制剂来阻断IJs的信号时，定向EC的百分比降低，而Paxillin的重新分布而不是整联蛋白β1被抑制。这些发现表明，IJ参与了通过FAK以外的信号传导途径进行循环拉伸的EC的定向。

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