水通道蛋白2 (AQP2)和血管加压素2型受体(V2R)在肾上皮细胞内吞作用:AQP2位于endocytosis-resistant膜域抗利尿激素治疗后。
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山楂Bouley等R, G, Russo LM,林HY,答哒,布朗D
水通道蛋白2 (AQP2)和血管加压素2型受体(V2R)在肾上皮细胞内吞作用:AQP2位于endocytosis-resistant膜域抗利尿激素治疗后。
细胞杂志。2006年4月,98 (4):215 - 32。
- PubMed ID
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16563128 (在PubMed]
- 文摘
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背景资料:水通道蛋白2 (AQP2)中扮演一个重要的副总裁(抗利尿激素)在肾水重吸收的调节作用。AQP2表示的金额主要细胞表面的结果从一个平衡AQP2在细胞内囊泡和AQP2在质膜上。副总裁质膜的平衡有利于转变,这允许渗透平衡发生和收集管腔之间的间隙空间。膜的积累AQP2可能源于胞外分泌VP-induced增加,内吞作用的减少,或两者兼而有之。在目前的研究中,我们进一步研究了AQP2积累在细胞表面,并比较其与V2R 2型受体(VP)贩卖使用细胞表达epitope-tagged AQP2 V2R。结果:V2R内吞作用和AQP2是独立事件,可以暂时分离和空间。内吞作用的破裂后副总裁靶细胞,当AQP2积累在细胞表面,主要是由于V2R的内化。增加引起的内吞作用不是forskolin,也导致膜AQP2积累腺苷酸环化酶的直接刺激。这表明营地海拔不是最初的主要原因,VP-induced内吞作用的过程。副总裁曝光后,AQP2不是与内化V2R位于核内体。 Instead, it remains at the cell surface in 'endocytosis-resistant' membrane domains, visualized by confocal imaging. After VP washout, AQP2 is progressively internalized with the fluid-phase marker FITC-dextran, indicating that VP washout releases an endocytotic block that maintains AQP2 at the cell surface. Finally, polarized application of VP to filter-grown cells shows that apical VP can induce basolateral endocytosis and V2R down-regulation, and vice versa. CONCLUSIONS: After VP stimulation of renal epithelial cells, AQP2 accumulates at the cell surface, while the V2R is actively internalized. This endocytotic block may involve a reduced capacity of phosphorylated AQP2 to interact with components of the endocytotic machinery. In addition, a complex cross-talk exists between the apical and basolateral plasma-membrane domains with respect to endocytosis and V2R down-regulation. This may be of physiological significance in down-regulating the VP response in the kidney in vivo.