Abstract
Aquaporin 3 (AQP3) is expressed in many tissues including the peritoneum and kidney. In cultured mesothelial cells, glucose up-regulates AQP3, which may be important for water transport through the peritoneal membrane. However, there has been no research into the role of AQP3 in human peritoneal mesothelial cell (HPMC) migration or peritoneal fibrosis. We investigated the effects of transforming growth factor-β1 (TGF-β1) on AQP3 expression in HPMCs. We also investigated the role of AQP3 in the peritoneal wound healing process in rats. Chronic exposure to glucose-containing solution increased peritoneal myofibroblasts, with TGF-β1 and AQP3 expression in a model of long-term peritoneal dialysis. In vitro, TGF-β1 induced AQP3 expression in HPMCs. AQP3 knockdown by small-interfering RNA inhibited TGF-β1-induced AQP3 and α-smooth muscle actin expression and also slowed HPMC migration. AQP3 overexpression induced faster migration of HPMCs. Treatment with an extracellular signal-regulated kinase inhibitor and p38 kinase inhibitor attenuated TGF-β1-induced AQP3 expression in HPMCs. These data suggest that TGF-β1 induces AQP3 and that AQP3 has a critical role in TGF-β-induced HPMC migration. These findings provide evidence of a novel role for AQP3 in peritoneal fibrosis and wound healing. The effect of TGF-β1 on AQP3 expression in HPMCs is mediated, at least in part, by ERK and p38 signaling.
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