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Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells

Title
Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells
Authors
Yu M.Shin H.-S.Lee H.K.Ryu D.-R.Kim S.-J.Choi K.-B.Kang D.-H.
Ewha Authors
강덕희최규복이현국김승정류동열
SCOPUS Author ID
강덕희scopus; 최규복scopus; 이현국scopus; 김승정scopus; 류동열scopus
Issue Date
2015
Journal Title
Kidney Research and Clinical Practice
ISSN
2211-9132JCR Link
Citation
vol. 34, no. 2, pp. 83 - 92
Keywords
AldosteroneEpithelial-to-mesenchymal transitionMesothelial cellPeritoneal dialysisPeritoneal fibrosis
Publisher
Elsevier
Indexed
SCOPUS; KCI scopus
Abstract
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.
DOI
10.1016/j.krcp.2015.03.005
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의학전문대학원 > 의학과 > Journal papers
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