BACKGROUND: Reactive oxygen species (ROS) may mediate pressure overload-induced myocardial hypertrophy. NADPH oxidase may be involved in this process, because its expression and activity are upregulated by pressure overload and because myocardial hypertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91phox catalytic subunit of NADPH oxidase. METHODS AND RESULTS: To test the role of NADPH oxidase-dependent ROS in mediating pressure overload-induced myocardial hypertrophy, we subjected transgenic mice lacking gp91phox to chronic pressure overload caused by constriction of the ascending aorta. Contrary to our hypothesis, neither myocardial hypertrophy nor NADPH-dependent superoxide generation was decreased in gp91phox-deficient mice after aortic constriction. Aortic constriction caused an exaggerated increase in p22phox and p47phox mRNA in gp91phox-deficient mice. CONCLUSIONS: These results indicate that gp91phox is not necessary for pressure overload-induced hypertrophy in the mouse and suggest the involvement of another source of ROS, possibly an NADPH oxidase that does not require the gp91phox subunit.
BACKGROUND:Reactive oxygen species (ROS) may mediate pressure overload-induced myocardial hypertrophy. NADPH oxidase may be involved in this process, because its expression and activity are upregulated by pressure overload and because myocardial hypertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91phox catalytic subunit of NADPH oxidase. METHODS AND RESULTS: To test the role of NADPH oxidase-dependent ROS in mediating pressure overload-induced myocardial hypertrophy, we subjected transgenic mice lacking gp91phox to chronic pressure overload caused by constriction of the ascending aorta. Contrary to our hypothesis, neither myocardial hypertrophy nor NADPH-dependent superoxide generation was decreased in gp91phox-deficient mice after aortic constriction. Aortic constriction caused an exaggerated increase in p22phox and p47phox mRNA in gp91phox-deficient mice. CONCLUSIONS: These results indicate that gp91phox is not necessary for pressure overload-induced hypertrophy in the mouse and suggest the involvement of another source of ROS, possibly an NADPH oxidase that does not require the gp91phox subunit.
Authors: Alison Cave; David Grieve; Sofian Johar; Min Zhang; Ajay M Shah Journal: Philos Trans R Soc Lond B Biol Sci Date: 2005-12-29 Impact factor: 6.237
Authors: Fuzhong Qin; Shannon Lennon-Edwards; Steve Lancel; Andreia Biolo; Deborah A Siwik; David R Pimentel; Gerald W Dorn; Y James Kang; Wilson S Colucci Journal: Circ Heart Fail Date: 2009-12-16 Impact factor: 8.790
Authors: An L Moens; Eiki Takimoto; Carlo G Tocchetti; Khalid Chakir; Djahida Bedja; Gianfranco Cormaci; Elizabeth A Ketner; Maulik Majmudar; Kathleen Gabrielson; Marc K Halushka; James B Mitchell; Shyam Biswal; Keith M Channon; Michael S Wolin; Nicholas J Alp; Nazareno Paolocci; Hunter C Champion; David A Kass Journal: Circulation Date: 2008-05-12 Impact factor: 29.690