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Release of ATP by TRPV4 activation is dependent upon the expression of AQP2 in renal cells

机译:TRPV4激活释放ATP的依赖AQP2在肾细胞的表达

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Increasing evidence indicates that aquaporins (AQPs) exert an influence in cell signaling by the interplay with the transient receptor potential vanilloid 4 (TRPV4) channel. We previously found that TRPV4 physically and functionally interacts with AQP2 in cortical collecting ducts (CCD) cells, favoring cell volume regulation and cell migration. Because TRPV4 was implicated in ATP release in several tissues, we investigated the possibility that TRPV4/AQP2 interaction influences ATP release in CCD cells. Using two CCD cell lines expressing or not AQP2, we measured extracellular ATP (ATPe) under TRPV4 activation and intracellular Ca~2+ under ATP addition. We found that AQP2 is critical for the release of ATP induced by TRPV4 activation. This ATP release occurs by an exocytic and a conductive route. ATPe, in turn, stimulates purinergic receptors leading to ATPe-induced ATP release by a Ca~2+-dependent mechanism. We propose that AQP2 by modulating Ca~2+ and ATP differently could explain AQP2-increased cell migration.
机译:越来越多的证据表明,水通道蛋白(aqp)施加在细胞信号产生影响瞬时受体的相互作用潜在的辣椒4 (TRPV4)通道。以前发现TRPV4身体和功能与AQP2皮质收集管道(CCD)细胞、支持细胞音量调节和细胞迁移。TRPV4在几个与ATP释放组织,我们调查的可能性TRPV4 / AQP2交互影响ATP释放CCD细胞。不是AQP2,我们测量细胞外ATP (ATPe)在TRPV4活化和细胞内Ca ~ 2 +在ATP。TRPV4引起的ATP的释放的关键激活。exocytic和导电的路线。刺激purinergic受体导致ATPe-induced Ca ~ 2 +端依赖ATP释放机制。Ca ~(2 +和ATP不同可以解释AQP2-increased细胞迁移。

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