Effects of sarcoplasmic reticulum Ca2-ATPase overexpression in postinfarction rat myocytes

Abstract

doi:10.1152/japplphysiol.00013.2005.—Previ-ous studies in adult myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) demonstrated abnormal contractility and intracellular Ca2 concentration ([Ca2]i) homeostasis and decreased sarcoplasmic reticulum Ca2-ATPase (SERCA2) expression and activity, but sarcoplasmic reticu-lum Ca2 leak was unchanged. In the present study, we investigated whether SERCA2 overexpression in MI myocytes would restore contraction and [Ca2]i transients to normal. Compared with sham-operated hearts, 3-wk MI hearts exhibited significantly higher left ventricular end-diastolic and end-systolic volumes but lower fractional shortening and ejection fraction, as measured by M-mode echocardiography. Seventy-two hours after adenovi-rus-mediated gene transfer, SERCA2 overexpression in 3-wk MI myocytes did not affect Na-Ca2 exchanger expression but restored the depressed SERCA2 levels toward those measured in sham myocytes. In addition, the reduced sarcoplasmic reticulum Ca2 uptake in MI myocytes was improve