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Aquaporin 11 a regulator of water efflux at retinal Müller glial cell surface decreases concomitant with immune-mediated gliosis

机译:视网膜Müller胶质细胞表面水流出调节剂水通道蛋白11减少并伴有免疫介导的神经胶质增生

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摘要

BackgroundMüller glial cells are important regulators of physiological function of retina. In a model disease of retinal inflammation and spontaneous recurrent uveitis in horses (ERU), we could show that retinal Müller glial cells significantly change potassium and water channel protein expression during autoimmune pathogenesis. The most significantly changed channel protein in neuroinflammatory ERU was aquaporin 11 (AQP11). Aquaporins (AQP, 13 members) are important regulators of water and small solute transport through membranes. AQP11 is an unorthodox member of this family and was assigned to a third group of AQPs because of its difference in amino acid sequence (conserved sequence is only 11 %) and especially its largely unknown function.
机译:背景穆勒神经胶质细胞是视网膜生理功能的重要调节剂。在模型性视网膜炎和马自发性复发性葡萄膜炎(ERU)的模型疾病中,我们可以证明视网膜Müller胶质细胞在自身免疫性发病机理中显着改变钾和水通道蛋白的表达。神经炎性ERU中变化最大的通道蛋白是水通道蛋白11(AQP11)。水通道蛋白(AQP,13个成员)是水和小溶质通过膜运输的重要调节剂。 AQP11是该家族的一个非传统成员,由于其氨基酸序列差异(保守序列仅为11%),尤其是其功能广泛未知,因此被分配给第三组AQP。

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