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Intracellular location of aquaporin-2 serine 269 phosphorylation and dephosphorylation in kidney collecting duct cells.
American Journal of Physiology-Renal Physiology ( IF 4.2 ) Pub Date : 2020-08-17 , DOI: 10.1152/ajprenal.00205.2020 Kit Yee Wong,Wei-Ling Wang,Shih-Han Su,Chin-Fu Liu,Ming-Jiun Yu
American Journal of Physiology-Renal Physiology ( IF 4.2 ) Pub Date : 2020-08-17 , DOI: 10.1152/ajprenal.00205.2020 Kit Yee Wong,Wei-Ling Wang,Shih-Han Su,Chin-Fu Liu,Ming-Jiun Yu
Aquaporin-2 (AQP2) is a vasopressin-regulated water channel protein responsible for water reabsorption by the kidney collecting ducts. Under control conditions, most AQP2 resides in the recycling endosomes of the principal cells where it answers to vasopressin with trafficking to the apical plasma membrane to increase water reabsorption. Upon vasopressin withdrawal, apical AQP2 retreats to the early endosomes before joining the recycling endosomes for the next vasopressin stimulation. Prior studies have demonstrated a role of AQP2 S269 phosphorylation in reducing AQP2 endocytosis thereby prolonging apical AQP2 retention. Here, we studied where in the cells S269 was phosphorylated and dephosphorylated in response to vasopressin versus withdrawal. In the mpkCCD collecting cells, Vps35 knockdown slowed vasopressin-induced apical AQP2 trafficking resulting in AQP2 accumulation in the recycling endosomes where S269 was phosphorylated. Rab7 knockdown that impaired AQP2 trafficking from the early to the recycling endosomes reduced vasopressin-induced S269 phosphorylation. Rab5 knockdown that impaired AQP2 endocytosis did not affect vasopressin-induced S269 phosphorylation. Upon vasopressin withdrawal, S269 was not dephosphorylated in Rab5 knockdown cells. In contrast, S269 dephosphorylation upon vasopressin withdrawal was completed in Rab7 or Vps35 knockdown cells. We conclude that S269 is dephosphorylated during Rab5-mediated AQP2 endocytosis before AQP2 joins the recycling endosomes upon vasopressin withdrawal. While in the recycling endosomes, AQP2 can be phosphorylated at S269 in response to vasopressin prior to apical trafficking.
中文翻译:
肾收集管细胞中aquaporin-2丝氨酸269磷酸化和去磷酸化的细胞内位置。
Aquaporin-2(AQP2)是一种加压素调节的水通道蛋白,负责肾脏收集导管对水的重吸收。在控制条件下,大多数AQP2驻留在主要细胞的再循环内体中,在其中它对血管加压素产生应答,并转运至顶质膜以增加水的重吸收。血管加压素退出后,顶端AQP2会退回到早期的内体,然后加入回收的内体以进行下一次加压素刺激。先前的研究表明AQP2 S269磷酸化在减少AQP2内吞作用,从而延长根尖AQP2保留中的作用。在这里,我们研究了细胞中S269的哪些位置被磷酸化和去磷酸化,以应对血管加压素相对于戒断反应。在mpkCCD收集单元中,Vps35击倒减慢了加压素诱导的顶端AQP2转运,导致AQP2在S269磷酸化的再循环内体中积累。Rab7击倒,削弱了从早期到回收内体的AQP2转运,降低了加压素诱导的S269磷酸化。Rab5敲低,损害AQP2内吞作用并不影响加压素诱导的S269磷酸化。血管加压素撤药后,S269在Rab5敲低细胞中未去磷酸化。相比之下,在Rab7或Vps35敲低的细胞中,加压素退出后S269的去磷酸化作用完成。我们得出的结论是,S269在Rab5介导的AQP2内吞过程中被去磷酸化,然后AQP2在血管加压素戒断后加入回收内体。在回收内体时
更新日期:2020-08-20
中文翻译:
肾收集管细胞中aquaporin-2丝氨酸269磷酸化和去磷酸化的细胞内位置。
Aquaporin-2(AQP2)是一种加压素调节的水通道蛋白,负责肾脏收集导管对水的重吸收。在控制条件下,大多数AQP2驻留在主要细胞的再循环内体中,在其中它对血管加压素产生应答,并转运至顶质膜以增加水的重吸收。血管加压素退出后,顶端AQP2会退回到早期的内体,然后加入回收的内体以进行下一次加压素刺激。先前的研究表明AQP2 S269磷酸化在减少AQP2内吞作用,从而延长根尖AQP2保留中的作用。在这里,我们研究了细胞中S269的哪些位置被磷酸化和去磷酸化,以应对血管加压素相对于戒断反应。在mpkCCD收集单元中,Vps35击倒减慢了加压素诱导的顶端AQP2转运,导致AQP2在S269磷酸化的再循环内体中积累。Rab7击倒,削弱了从早期到回收内体的AQP2转运,降低了加压素诱导的S269磷酸化。Rab5敲低,损害AQP2内吞作用并不影响加压素诱导的S269磷酸化。血管加压素撤药后,S269在Rab5敲低细胞中未去磷酸化。相比之下,在Rab7或Vps35敲低的细胞中,加压素退出后S269的去磷酸化作用完成。我们得出的结论是,S269在Rab5介导的AQP2内吞过程中被去磷酸化,然后AQP2在血管加压素戒断后加入回收内体。在回收内体时