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Mechanisms of epithelial-mesenchymal transition of peritoneal mesothelial cells during peritoneal dialysis

Title
Mechanisms of epithelial-mesenchymal transition of peritoneal mesothelial cells during peritoneal dialysis
Authors
Hi B.L.Ha H.
Ewha Authors
하헌주
SCOPUS Author ID
하헌주scopus
Issue Date
2007
Journal Title
Journal of Korean Medical Science
ISSN
1011-8934JCR Link
Citation
vol. 22, no. 6, pp. 943 - 945
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
A growing body of evidence indicates that epithelial-mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMC) may play an important role in the development and progression of peritoneal fibrosis during long-term peritoneal dialysis (PD) leading to failure of peritoneal membrane function. Here, we review our own observations and those of others on the mechanisms of EMT of HPMC and suggest potential therapeutic strategies to prevent EMT and peritoneal fibrosis during long-term PD. We found that high glucose and H 2O2 as well as transforming growth factor-β1 (TGF-β1) induced EMT in HPMC and that high glucose-induced EMT was blocked not only by inhibition of TGF-β1 but also by antioxidants or inhibitors of mitogen-activated protein kinases (MAPK). Since MAPKs are downstream target molecules of reactive oxygen species (ROS), these data suggest that high glucose-induced generation of ROS and subsequent MAPK activation mediate high glucose-induced EMT in HPMC. We and others also observed that bone morphogenetic protein-7 (BMP-7) prevented EMT in HPMC. Glucose degradation products (GDP) were shown to play a role in inducing EMT. Involvement of a mammalian target of rapamycin (mTOR) in TGF-β1-induced EMT has also been proposed in cultured HPMC. A better understanding of the precise mechanisms involved in EMT of HPMC may provide new therapeutic strategies for inhibiting peritoneal fibrosis in long-term PD patients. Copyright © The Korean Academy of Medical Sciences.
DOI
10.3346/jkms.2007.22.6.943
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약학대학 > 약학과 > Journal papers
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