Lack of microsomal prostaglandin E(2) synthase-1 in bone marrow-derived myeloid cells impairs left ventricular function and increases mortality after acute myocardial infarction.

Background—Microsomal prostaglandin E2 synthase-1 (mPGES-1), encoded by the Ptges gene, catalyzes prostaglandin E2 biosynthesis and is expressed by leukocytes, cardiac myocytes, and cardiac fibroblasts. Ptges−/− mice develop more left ventricle (LV) dilation, worse LV contractile function, and higher LV end-diastolic pressure than Ptges+/+ mice after myocardial infarction. In this study, we define the role of mPGES-1 in bone marrow–derived leukocytes in the recovery of LV function after coronary ligation. Methods and Results—Cardiac structure and function in Ptges+/+ mice with Ptges+/+ bone marrow (BM+/+) and Ptges+/+ mice with Ptges−/− BM (BM−/−) were assessed by morphometric analysis, echocardiography, and invasive hemodynamics before and 7 and 28 days after myocardial infarction. Prostaglandin levels and prostaglandin biosynthetic enzyme gene expression were measured by liquid chromatography–tandem mass spectrometry and real-time polymerase chain reaction, immunoblotting, immunohistochemistry, and immu...