Impaired In Vivo Reendothelialization Capacity of Endothelial Progenitor Cells of Patients with Type-2 Diabetes Is Restored by PPAR-Gamma Agonist Rosiglitazone: Role of NAD(P)H Oxidase and Nitric Oxide
DOI: 10.1016/j.vph.2006.08.116 Conference: International Vascular Biology Meeting
Available from: imr.sagepub.com
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ABSTRACT: This study investigated the effects of the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone (RGZ) on cardiac fibroblast proliferation, nitric oxide content and connective tissue growth factor (CTGF) expression following incubation with advanced glycation end-products (AGEs). Cultured neonatal rat cardiac fibroblasts were incubated with various concentrations of AGEs for 48 h. Cells were also incubated with 200 mg/l AGEs plus various concentrations of RGZ. Cardiac fibroblast proliferation and cell cycle status were detected using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Western blotting was used to measure the expression of CTGF and nitric oxide content was evaluated using a nitrate reductase assay. AGEs significantly accelerated proliferation, increased CTGF expression and decreased nitric oxide production in cardiac fibroblasts. These effects of AGEs were inhibited by RGZ in a dose-dependent manner. Treatment with RGZ could be a valuable therapeutic approach in diabetic patients with myocardial fibrosis.
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