Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox.

Maytin M, Siwik DA, Ito M, Xiao L, Sawyer DB, Liao R, Colucci WS
Circulation. 2004 109 (9): 1168-71

PMID: 14981002 · DOI:10.1161/01.CIR.0000117229.60628.2F

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.

MeSH Terms (12)

Animals Aorta Cardiomegaly Constriction Glutathione Mice Mice, Inbred C57BL Mice, Transgenic NADPH Oxidases Pressure Protein Subunits RNA, Messenger

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