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Background . Peritoneal dialysis (PD) can induce fibrosis and functional alterations in PD patients' peritoneal membranes, due to long-term unphysiological dialysate exposure, partially occurring via triggering of epithelial-to-mesenchymal transition (EMT) in peritoneal mesothelial cells (MCs). Vitamin D can ameliorate these negative effects; however, the mechanism remains unexplored. Therefore, we investigated its possible links to MCs EMT inhibition.  Methods . Peritoneal fibrosis was established in Sprague-Dawley rats by chlorhexidine gluconate (CG) intraperitoneal injection for 21 days, with and without 1 α ,25(OH) 2 D 3  treatment. Morphological and functional evaluation and western blot analysis of EMT marker were performed upon peritoneum tissue.  In vitro  study was also performed in a primary human peritoneal MC culture system; MCs were incubated with transforming growth factor- β 1 (TGF- β 1) in the absence or presence of 1 α ,25(OH) 2 D 3 . EMT marker expression, migration activities, and cytoskeleton redistribution of MCs were determined.  Results . 1 α ,25(OH) 2 D 3  ameliorated CG-induced morphological and functional deterioration in animal model, along with CG-induced upregulation of  α -SMA and downregulation of E-cadherin expression. Meanwhile, 1 α ,25(OH) 2 D 3  also ameliorated TGF- β 1-induced decrease in E-cadherin expression, increase in Snai1 and  α -SMA expression, intracellular F-actin redistribution, and migration activity  in vitro .  Conclusion . 1 α ,25(OH) 2 D 3  can ameliorate CG-induced peritoneal fibrosis and attenuate functional deterioration through inhibiting MC EMT.

biomed research international

Vitamin D Can Ameliorate Chlorhexidine Gluconate-Induced Peritoneal Fibrosis and Functional Deterioration through the Inhibition of Epithelial-to-Mesenchymal Transition of Mesothelial Cells