抗利尿激素调控肾集管细胞水通道蛋白-2的研究进展。

Pub Date : 2015-06-01 Epub Date: 2015-06-30 DOI:10.5049/EBP.2015.13.1.1
Eui-Jung Park, Tae-Hwan Kwon
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引用次数: 30

摘要

肾集管是调节机体水盐平衡的重要肾小管段。精氨酸抗利尿素(AVP)通过抗利尿素v2受体(V2R)调节收集管细胞的水重吸收。AVP通过水通道蛋白-2 (AQP2)和水通道蛋白-3 (AQP3)增加集管细胞的渗透性。AVP诱导AQP2在肾集管主细胞的顶端靶向和AQP2基因的转录。AQP2转运至集管主细胞顶质膜的信号转导途径包括AQP2磷酸化、RhoA磷酸化、肌动蛋白解聚和钙动员等,水平衡紊乱中AQP2蛋白丰度的变化已被广泛研究。这些研究阐明了体内水分平衡的细胞和分子机制,为体内水分平衡失调的治疗提供了基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A Minireview on Vasopressin-regulated Aquaporin-2 in Kidney Collecting Duct Cells.

A Minireview on Vasopressin-regulated Aquaporin-2 in Kidney Collecting Duct Cells.
The kidney collecting duct is an important renal tubular segment for the regulation of body water and salt homeostasis. Water reabsorption in the collecting duct cells is regulated by arginine vasopressin (AVP) via the vasopressin V2-receptor (V2R). AVP increases the osmotic water permeability of the collecting duct cells through aquaporin-2 (AQP2) and aquaporin-3 (AQP3). AVP induces the apical targeting of AQP2 and transcription of AQP2 gene in the kidney collecting duct principal cells. The signaling transduction pathways resulting in the AQP2 trafficking to the apical plasma membrane of the collecting duct principal cells, include AQP2 phosphorylation, RhoA phosphorylation, actin depolymerization and calcium mobilization, and the changes of AQP2 protein abundance in water balance disorders have been extensively studied. These studies elucidate the underlying cellular and molecular mechanisms of body water homeostasis and provide the basis for the treatment of body water balance disorders.
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