NADPH oxidase activation played a critical role in the oxidative stress process in stable coronary artery disease.

作者：Jiefang Zhang, Meihui Wang, Zhengwei Li, Xukun Bi, Jia‐Le Song, Shaoxiang Weng, Guosheng Fu · 发表于：PubMed · 年份：2016 · 被引用次数：15 · 研究领域：Neutrophil, Myeloperoxidase and Oxidative Mechanisms、Atherosclerosis and Cardiovascular Diseases、Lipid metabolism and disorders

OBJECTIVES: The study was designed to investigate the oxidative stress levels of endothelial progenitor cells (EPCs) in stable coronary artery disease (CAD) and to explore the underlying mechanisms of NADPH oxidase activation and subsequent EPCs dysfunction. METHODS: using immunofluorescence. The in vivo angiogenesis capacity was evaluated using immunofluorescence by transplanting EPCs into a rat hind limb ischemia model. The PKC inhibitor GÖ-6983 was used to determine the role of PKC in NADPH oxidase activation. RESULTS: membrane translocation increased in CAD group vs controls. These effects were resolved by NADPH oxidase inhibition. Up-regulation of PKCα/β2 was found in EPCs from CAD subjects, PKC inhibition GÖ-6983 could reduce the expression and activity of NADPH oxidation. CONCLUSIONS: membrane translocation played a critical role in the initiation and progression of CAD, and the PKCα/β2 signaling pathway might be involved.