Reduced Cardiac Remodeling and Function in Cardiac-Specific EP 4 Receptor Knockout Mice With Myocardial Infarction

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Abstract
We have shown previously that cyclooxygenase-2 inhibition reduces cardiac hypertrophy and fibrosis postmyocardial infarction (MI) in a mouse model and that prostaglandin E2 stimulates cardiomyocyte hypertrophy in vitro through its EP4 receptor. Because the role of cardiac myocyte EP4 in cardiac function and hypertrophy in vivo is unknown, we generated mice lacking EP4 only in cardiomyocytes (CM- EP4 knockout [KO]). Twelve- to 14-week–old mice were evaluated using echocardiography and histology. There were no differences in ejection fraction, myocyte cross-sectional area, and interstitial collagen fraction between KO mice and littermate controls. To test the hypothesis that EP4 is involved in cardiac remodeling after MI, we induced MI by ligating the left anterior descending coronary artery. Two weeks later, the mice were subjected to echocardiography, and hearts were removed for histology and Western blot. There was no difference in infarct size between KO mice and controls; however, KO mice showed less m...