Angiotensin II increases ROS production in cardiac fibroblasts by inducing p22phox over-expression.
- Author:
Rong GUO
1
;
Juan ZHOU
;
Xiu-ling DENG
;
Guang-dao GAO
;
Xiao-ying JIANG
;
Yuan-xi LIN
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Animals, Newborn; Cells, Cultured; Fibroblasts; metabolism; Myocardium; cytology; NADPH Oxidases; metabolism; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; metabolism
- From: Journal of Southern Medical University 2009;29(2):202-204
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the changes in the reactive oxygen species (ROS) in rat cardiac fibroblasts exposed to angiotensin II (Ang II) treatment and explore the possible pathways that mediate ROS production.
METHODSIn vitro cultured fetal rat cardiac fibroblasts treated with apocynin (APO, 100 micromol/L), Ang II (10(-7) mol/L), or APO+Ang II (10(-7) mol/L Ang II was added 1 h after 100 micromol/L APO), and the ROS levels and p22phox expression in the cells were detected using fluorescent microscope and immunohistochemistry, respectively.
RESULTSCompared with the normal control cells, Ang II treatment of the cardiac fibroblasts resulted in significantly increased ROS production, the effect of which was inhibited by the application of APO. p22phox expression was hardly detected by immunohistochemistry in the control cells, but over-expressed in AngII-treated cells. APO substantially decreased the over-expression of p22phox induced by Ang II.
CONCLUSIONAng II increases ROS production in fetal rat cardiac fibroblasts probably by inducing p22phox over-expression.
