Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 강덕희 | * |
dc.contributor.author | 최규복 | * |
dc.contributor.author | 이현국 | * |
dc.contributor.author | 김승정 | * |
dc.contributor.author | 류동열 | * |
dc.date.accessioned | 2016-08-29T12:08:12Z | - |
dc.date.available | 2016-08-29T12:08:12Z | - |
dc.date.issued | 2015 | * |
dc.identifier.issn | 2211-9132 | * |
dc.identifier.other | OAK-15120 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/230630 | - |
dc.description.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. | * |
dc.language | English | * |
dc.publisher | Elsevier | * |
dc.subject | Aldosterone | * |
dc.subject | Epithelial-to-mesenchymal transition | * |
dc.subject | Mesothelial cell | * |
dc.subject | Peritoneal dialysis | * |
dc.subject | Peritoneal fibrosis | * |
dc.title | Effect of aldosterone on epithelial-to-mesenchymal transition of human peritoneal mesothelial cells | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 34 | * |
dc.relation.index | SCOPUS | * |
dc.relation.index | KCI | * |
dc.relation.startpage | 83 | * |
dc.relation.lastpage | 92 | * |
dc.relation.journaltitle | Kidney Research and Clinical Practice | * |
dc.identifier.doi | 10.1016/j.krcp.2015.03.005 | * |
dc.identifier.scopusid | 2-s2.0-84937516921 | * |
dc.author.google | Yu M. | * |
dc.author.google | Shin H.-S. | * |
dc.author.google | Lee H.K. | * |
dc.author.google | Ryu D.-R. | * |
dc.author.google | Kim S.-J. | * |
dc.author.google | Choi K.-B. | * |
dc.author.google | Kang D.-H. | * |
dc.contributor.scopusid | 강덕희(17233695600) | * |
dc.contributor.scopusid | 최규복(36096388100) | * |
dc.contributor.scopusid | 이현국(8861888600) | * |
dc.contributor.scopusid | 김승정(8619054500) | * |
dc.contributor.scopusid | 류동열(7103144218;56997547400;56669926200) | * |
dc.date.modifydate | 20240419142141 | * |