| First Author | Maytin M | Year | 2004 |
| Journal | Circulation | Volume | 109 |
| Issue | 9 | Pages | 1168-71 |
| PubMed ID | 14981002 | Mgi Jnum | J:131488 |
| Mgi Id | MGI:3773804 | Doi | 10.1161/01.CIR.0000117229.60628.2F |
| Citation | Maytin M, et al. (2004) Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox. Circulation 109(9):1168-71 |
| abstractText | 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. |
