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J Mol Cell Cardiol. 2010 Jul;49(1):88-94. doi: 10.1016/j.yjmcc.2010.01.021. Epub 2010 Feb 17.

Compensatory hypertrophy induced by ventricular cardiomyocyte-specific COX-2 expression in mice.

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Department of Anesthesiology, David Geffen School of Medicine, University of California - Los Angeles, Los Angeles, CA 90095, USA.


Cyclooxygenase-2 (COX-2) is an important mediator of inflammation in stress and disease states. Recent attention has focused on the role of COX-2 in human heart failure and diseases owing to the finding that highly specific COX-2 inhibitors (i.e., Vioxx) increased the risk of myocardial infarction and stroke in chronic users. However, the specific impact of COX-2 expression in the intact heart remains to be determined. We report here the development of a transgenic mouse model, using a loxP-Cre approach, which displays robust COX-2 overexpression and subsequent prostaglandin synthesis specifically in ventricular myocytes. Histological, functional, and molecular analyses showed that ventricular myocyte specific COX-2 overexpression led to cardiac hypertrophy and fetal gene marker activation, but with preserved cardiac function. Therefore, specific induction of COX-2 and prostaglandin in vivo is sufficient to induce compensated hypertrophy and molecular remodeling.

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