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Regulation of the epithelial Na+/H+ exchanger isoform by the cytoskeleton [Review]

机译：细胞骨架对上皮Na + / H +交换异构体的调节[综述]

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摘要

Members of the Na+/H+ exchanger (NHE) family mediate electroneutral countertransport of H+ for Na+ across cellular membranes. The six known isoforms mediate transepithelial Na+ transport processes and housekeeping functions such as the regulation of cellular and organellar pH and volume. NHE3 is found primarily in the apical membrane of epithelial cells of the kidney and gastrointestinal tract, where it mediates Na+ (re)absorption. Its fine regulation, whether by hormones that utilize cAMP as a signalling mechanism, or by physical parameters such as the cell volume, provides the adjustments necessary for the maintenance of systemic salt and fluid balance. Although the exact molecular mechanism of this control is unknown, two major modes of regulation have been invoked: 1) alteration of the number of cell surface transporters by changes in the rate of endocytosis and/or exocytosis and 2) regulation of the intrinsic activity of the individual exchangers. NHE3 requires an intact cytoskeleton for its optimal function. Pharmacological interference with actin polymerization or myosin phosphorylation markedly inhibits the exchanger, without altering the number of transporters exposed at the surface. This effect is isoform specific and is mediated by the cytoplasmic tail of the transporter. The small GTP-binding protein, RhoA and its downstream effector, Rho kinase regulate NHE3, possibly by controlling the level of myosin phosphorylation, that in turn determines the organization of actin. The cytoskeleton may not only be involved in the maintenance of the basal rate of transport, but is also likely to sense physical alterations and transmit signals to modulate NHE3 activity, thus providing fast and effective control of the exchanger. Copyright (C) 2000 S. Karger AG, Basel. [References: 45]
机译：Na + / H +交换子（NHE）家族的成员介导H +对Na +跨细胞膜的电中性逆转运。六种已知的同工型可介导跨上皮的Na +转运过程和管家功能，例如调节细胞和细胞器的pH和体积。 NHE3主要存在于肾脏和胃肠道上皮细胞的顶膜中，在其中介导Na +（再）吸收。无论是通过利用cAMP作为信号传导机制的激素，还是通过诸如细胞体积的物理参数，它的精细调节都为维持全身性盐和体液平衡提供了必要的调节。尽管尚不清楚该控制的确切分子机制，但已调用了两种主要的调节模式：1）通过改变内吞和/或胞吐作用的速率改变细胞表面转运蛋白的数量，以及2）调节内在活性。各个交换器。 NHE3需要完整的细胞骨架才能发挥最佳功能。肌动蛋白聚合或肌球蛋白磷酸化的药理学干扰显着抑制了交换子，而没有改变暴露于表面的转运蛋白的数量。该作用是同工型特异性的，并由转运蛋白的细胞质尾部介导。较小的GTP结合蛋白RhoA及其下游效应子Rho激酶可能通过控制肌球蛋白的磷酸化水平来调节NHE3，进而决定肌动蛋白的组织。细胞骨架不仅可能参与基本运输速率的维持，而且还可能感知物理变化并传输信号以调节NHE3活性，从而提供对交换子的快速有效控制。版权所有（C）2000 S.Karger AG，巴塞尔。 [参考：45]

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