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水通道蛋白的表达调控与转运

Expression Regulation and Trafficking of Aquaporins.

作者信息

Zhao Xiaoduo, Liang Baien, Li Chunling, Wang Weidong

机构信息

Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

Department of Physiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

出版信息

Adv Exp Med Biol. 2023;1398:39-51. doi: 10.1007/978-981-19-7415-1_3.

Abstract

Aquaporins (AQPs) mediate the bidirectional water flow driven by an osmotic gradient. Either gating or trafficking allows for rapid and specific AQP regulation in a tissue-dependent manner. The regulatory mechanisms of AQP2 are discussed mainly in this chapter, as the mechanisms controlling the regulation and trafficking of AQP2 have been very well studied. The targeting of AQP2 to the apical plasma membrane of collecting duct principal cells is mainly regulated by the action of arginine vasopressin (AVP) on the type 2 AVP receptor (V2R), which cause increased intracellular cAMP or elevated intracellular calcium levels. Activation of these intracellular signaling pathways results in vesicles bearing AQP2 transport, docking and fusion with the apical membrane, which increase density of AQP2 on the membrane. The removal of AQP2 from the membrane requires dynamic cytoskeletal remodeling. AQP2 is degraded through the ubiquitin proteasome pathway and lysosomal proteolysis pathway. Finally, we review updated findings in transcriptional and epigenetic regulation of AQP2.

摘要

水通道蛋白(AQPs)介导由渗透梯度驱动的双向水流。门控或转运都能以组织依赖的方式实现对水通道蛋白的快速且特异性调节。本章主要讨论水通道蛋白2(AQP2)的调节机制,因为控制AQP2调节和转运的机制已得到充分研究。集合管主细胞顶质膜上AQP2的靶向定位主要受精氨酸加压素(AVP)作用于2型AVP受体(V2R)的调控,这会导致细胞内cAMP增加或细胞内钙水平升高。这些细胞内信号通路的激活会使携带AQP2的囊泡发生转运、对接并与顶膜融合,从而增加膜上AQP2的密度。将AQP2从膜上去除需要动态的细胞骨架重塑。AQP2通过泛素蛋白酶体途径和溶酶体蛋白水解途径降解。最后,我们综述了AQP2转录和表观遗传调控方面的最新研究成果。

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