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- W3692553 abstract "We had reported a transgenic (Tg) mouse model with cardiac-specific overexpression of a dominant-negative (DN) mutant (V204A) of NADPH oxidase (NOX) subunit p67 phox that inhibits NOX activity. We showed that transverse aortic constriction (TAC)-induced cardiac hypertrophy was significantly attenuated in the Tg mice, but not in wild type (WT) mice. Since TAC had been reported to increase mouse myocardial reactive oxygen species (ROS) level, we thus tested if the myocardial ROS contributed to the above difference between WT and Tg. Age (10-12 weeks)-, body weight (BW)-matched Tg and WT C57BL/6 male mice were subjected to TAC or sham operation. Cardiac hypertrophy were confirmed 4-week post-TAC by echocardiography, heart weight/BW ratio, and fetal gene expression. Freshly isolated hearts were perfused and the left ventricle (LV) ROS level was determined using chemiluminescence method. Surprisingly, we found that the WT-TAC mouse heart showed consistently decreased ROS level (42±2% ↓, p phox in regulation of TAC-induced myocardial ROS generation and antioxidants expression. In summary, our data show that NOX/p67 phox regulates pressure-overload-induced cardiac oxidative stress and myocardial expression of antioxidants SOD3 and Trx1." @default.
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- W3692553 date "2011-11-22" @default.
- W3692553 modified "2023-09-24" @default.
- W3692553 title "Abstract 17477: Role of NADPH Oxidase Subunit p67phox in Regulation of Pressure-Overload-Induced Cardiac Hypertrophic Oxidative Stress and Antioxidant Gene Expression" @default.
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