Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2015 (2015), Article ID 595030, 12 pages
Research Article

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

1Division of Nephrology, Department of Internal Medicine, E-DA Hospital, I-Shou University, Kaohsiung, Taiwan
2Institute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan
3School of Medicine for International Students, I-Shou University, Kaohsiung, Taiwan
4Division of Nephrology, Department of Medicine, Hsin-Jen Hospital, New Taipei City, Taiwan
5Department of Laboratory Medicine, E-DA Hospital, I-Shou University, Kaohsiung, Taiwan
6Division of Colorectal Surgery, Department of Surgery, E-DA Hospital, I-Shou University, Kaohsiung, Taiwan
7Department of Neurosurgery, E-DA Hospital, I-Shou University, Kaohsiung, Taiwan
8Department of Medical Education, I-Shou University, Kaohsiung, Taiwan
9Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan

Received 29 March 2015; Accepted 12 July 2015

Academic Editor: Robert Beelen

Copyright © 2015 Yi-Che Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 1α,25(OH)2D3 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-β1 (TGF-β1) in the absence or presence of 1α,25(OH)2D3. EMT marker expression, migration activities, and cytoskeleton redistribution of MCs were determined. Results. 1α,25(OH)2D3 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, 1α,25(OH)2D3 also ameliorated TGF-β1-induced decrease in E-cadherin expression, increase in Snai1 and α-SMA expression, intracellular F-actin redistribution, and migration activity in vitro. Conclusion. 1α,25(OH)2D3 can ameliorate CG-induced peritoneal fibrosis and attenuate functional deterioration through inhibiting MC EMT.