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首页> 外文期刊>American Journal of Physiology >Regulation of MDCK cell-substratum adhesion by RhoA and myosin light chain kinase after ATP depletion
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Regulation of MDCK cell-substratum adhesion by RhoA and myosin light chain kinase after ATP depletion

机译：ATP耗竭后RhoA和肌球蛋白轻链激酶调节MDCK细胞-基质粘附

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摘要

The attachment of epithelial cells to the extracellular matrix substratum is essential for their differentiation and polarization. Despite this, the precise adhesion mechanism and its regulation are poorly understood. In the kidney, an ischemic insult causes renal tubular epithelial cells to detach from the basement membrane, even though they remain viable. To understand this phenomenon, and to probe the regulation of epithelial cell attachment, we used a model system consisting of newly adherent Madin-Darby canine kidney (MDCK) cells subjected to ATP depletion to mimic ischemic injury. We found that MDCK cells detach from collagen I after 60 min of ATP depletion but reattach when resupplied with glucose. Detachment is not caused by degradation or endocytosis of beta_1-integrins, which mediate attachment to collagen I. Basal actin filaments and paxillin-containing adhesion complexes are disrupted by ATP depletion and quickly reform on glucose repletion.
机译：上皮细胞对细胞外基质基质的附着对其分化和极化至关重要。尽管如此，人们对精确的粘合机理及其调节却知之甚少。在肾脏中，缺血性损伤会导致肾小管上皮细胞从基底膜分离，即使它们仍然可以存活。为了了解这种现象，并探讨上皮细胞附着的调控，我们使用了一个模型系统，该模型系统由新附着的Madin-Darby犬肾（MDCK）细胞组成，该细胞经过ATP耗竭以模拟缺血性损伤。我们发现，ATP耗竭60分钟后，MDCK细胞会从胶原蛋白I分离，但在补充葡萄糖后会重新附着。分离不是由β_1整合素的降解或内吞作用引起的，介导与胶原蛋白I的附着。ATP耗竭破坏了基础肌动蛋白丝和含paxillin的粘附复合物，并迅速恢复了葡萄糖的摄取。

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