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Angiotensin II mediates high glucose-induced TGF-beta 1 and fibronectin upregulation in HPMC through reactive oxygen species

Title
Angiotensin II mediates high glucose-induced TGF-beta 1 and fibronectin upregulation in HPMC through reactive oxygen species
Authors
Noh, HHa, HYu, MRKim, YOKim, JHLee, HB
Ewha Authors
하헌주
SCOPUS Author ID
하헌주scopus
Issue Date
2005
Journal Title
PERITONEAL DIALYSIS INTERNATIONAL
ISSN
0896-8608JCR Link
Citation
vol. 25, no. 1, pp. 38 - 47
Keywords
high glucosefibronectinperitoneal fibrosisreactive oxygen speciesrenin-angiotensin systemTGF-beta 1
Publisher
MULTIMED INC
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Objective: To demonstrate the presence of an independent renin-angiotensin system (RAS) in the peritoneum and to determine the role of locally produced angiotensin (Ang) II in high gLucose-induced upregulation of transforming growth factor (TGF)-beta 1 and fibronectin by human peritoneal mesothelial cells (HPMC). Methods: In cultured HPMC, the expression of mRNAs for angiotensinogen, angiotensin-converting enzyme (ACE), Ang II type 1 receptor (AT1), and TGF-beta 1 was evaluated by real-time polymerase chain reaction; ACE, AT1, and fibronectin proteins by Western blot analysis; and Ang 1, Ang II, and TGF-beta 1 proteins by ELISA. Dichlorofluorscein (DCF)-sensitive cellular reactive oxygen species (ROS) were measured by fluorometry. Results: HPMC constitutively expressed all the components of RAS, and 50 mmoL/L D-glucose (high glucose) significantly increased angiotensinogen, ACE, and AT1 m RNAs and ACE, AT1, and Ang II proteins. Ang 11 increased TGF-beta 1 and fibronectin protein expression and DCF-sensitive cellular ROS. Losartan prevented Ang II-induced increase in cellular ROS. Both Losartan and captopril inhibited high gLucose-induced upregulation of TGF-beta 1 and fibronectin expression in HPMC in a dose-dependent manner. Antioxidant catalase and NADPH oxidase inhibitor diphenyleneiodinium effectively inhibited Ang 11-induced TGF-beta 1 and fibronectin protein expression. Conclusions: The present data demonstrate that HPMC constitutively express RAS, that Ang II produced by HPMC mediates high gLucose-induced upregulation of TGF-beta 1 and fibronectin expression, and that Ang II-induced TGF-beta 1 and fibronectin expression in HPMC is mediated by NADPH oxidase-dependent ROS. These data suggest that Locally produced Ang II and ROS in the peritoneum may be potential therapeutic targets in peritoneal fibrosis during long-term peritoneal dialysis.
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약학대학 > 약학과 > Journal papers
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