Ischemia-induced loss of epithelial polarity: potential role of the actin cytoskeleton.
Ischemia-induced loss of epithelial polarity: potential role of the actin cytoskeleton.
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DOI：
10.1152/ajprenal.1991.260.6.f769
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发表时间：
1991-06
期刊：
影响因子：
--
通讯作者：
B. Molitoris
中科院分区：
文献类型：
--
作者：
B. Molitoris
近端小管细胞在从肾小球滤液重吸收离子、水和溶质中起主要作用。这在很大程度上是通过极化成结构上、生物化学上和生理上不同的顶端和基底外侧膜结构域的表面膜来实现的，所述顶端和基底外侧膜结构域由细胞连接复合物分离。这些独特的膜结构域的建立和维护是至关重要的近端肾小管细胞的正常功能，是依赖于皮质肌动蛋白细胞间隙表面膜的相互作用。缺血导致顶侧和基底侧表面膜脂质和蛋白质极性的持续时间依赖性损失。这种表面膜极性的丧失与皮质肌动蛋白微丝网络的破坏和细胞紧密连接的开放有关。然后，表面膜脂质和蛋白质在膜双层内自由地横向扩散到交替的膜结构域中。在功能上，缺血诱导的上皮极性丧失部分地导致钠和葡萄糖重吸收减少。随着恢复，近端小管细胞经历表面膜的重塑，使得独特的顶侧和基底侧膜域被重建，从而允许正常的细胞功能恢复。
Proximal tubule cells play a major role in the reabsorption of ions, water, and solutes from the glomerular filtrate. This is accomplished, in large part, by a surface membrane polarized into structurally, biochemically, and physiologically distinct apical and basolateral membrane domains separated by cellular junctional complexes. Establishment and maintenance of these unique membrane domains is essential for the normal functioning of proximal tubular cells and is dependent on cortical actin cytoskeletal-surface membrane interactions. Ischemia results in the duration-dependent loss of apical and basolateral surface membrane lipid and protein polarity. This loss of surface membrane polarity is associated with disruption of the cortical actin microfilament network and the opening of cellular tight junctions. Surface membrane lipids and proteins are then free to diffuse laterally within the membrane bilayer into the alternate membrane domain. Functionally, ischemia-induced loss of epithelial polarity is, in part, responsible for reduced sodium and glucose reabsorption. With recovery, proximal tubule cells undergo remodeling of the surface membrane such that the unique apical and basolateral membrane domains are reestablished allowing normal cellular function to return.