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Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells
- Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells
- Yu M.; Shin H.-S.; Lee H.K.; Ryu D.-R.; Kim S.-J.; Choi K.-B.; Kang D.-H.
- Ewha Authors
- 강덕희; 최규복; 이현국; 김승정; 류동열
- SCOPUS Author ID
- 강덕희; 최규복; 이현국; 김승정; 류동열
- Issue Date
- Journal Title
- Kidney Research and Clinical Practice
- vol. 34, no. 2, pp. 83 - 92
- Aldosterone; Epithelial-to-mesenchymal transition; Mesothelial cell; Peritoneal dialysis; Peritoneal fibrosis
- SCOPUS; KCI
- Background Peritoneal fibrosis is one of the major causes of technical failure in patients on peritoneal dialysis. Epithelial-to-mesenchymal transition (EMT) of the peritoneum is an early and reversible mechanism of peritoneal fibrosis. Human peritoneal mesothelial cells (HPMCs) have their own renin-angiotensin-aldosterone system (RAAS), however, it has not been investigated whether aldosterone, an end-product of the RAAS, induces EMT in HPMCs, and which mechanisms are responsible for aldosterone-induced EMT. Methods EMT of HPMCs was evaluated by comparing the expression of epithelial cell marker, E-cadherin, and mesenchymal cell marker, α-smooth muscle actin after stimulation with aldosterone (1-100nM) or spironolactone. Activation of extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) and generation of reactive oxygen species (ROS) were assessed by western blotting and 2′,7′-dichlorofluororescein diacetate staining, respectively. The effects of MAPK inhibitors or antioxidants (N-acetyl cysteine, apocynin, and rotenone) on aldosterone-induced EMT were evaluated. Results Aldosterone induced EMT in cultured HPMCs, and spironolactone blocked aldosterone-induced EMT. Aldosterone induced activation of both ERK1/2 and p38 MAPK from 1 hour. Either PD98059, an inhibitor of ERK1/2, or SB20358, an inhibitor of p38 MAPK, attenuated aldosterone-induced EMT. Aldosterone induced ROS in HPMCs from 5 minutes, and antioxidant treatment ameliorated aldosterone-induced EMT. N-acetyl cysteine and apocynin alleviated activation of ERK and p38 MAPK. Conclusion Aldosterone induced EMT in HPMCs by acting through the mineralocorticoid receptor. Aldosterone-induced generation of ROS followed by activation of ERK, and p38 MAPK served as one of the mechanisms of aldosterone-induced EMT of HPMCs. © 2015. The Korean Society of Nephrology. Published by Elsevier. All rights reserved.
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