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Am J Physiol Cell Physiol 280: C573-C580, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 3, C573-C580, March 2001

Redistribution and abnormal activity of phospholipase A2 isoenzymes in postinfarct congestive heart failure

Jane McHowat1, Paramjit S. Tappia2, Song-Yan Liu2, Raetreal McCrory1, and Vincenzo Panagia2,dagger

1 Department of Pathology, St. Louis University Medical School, St. Louis, Missouri 63104; and 2 Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Departments of Human Anatomy and Cell Science and Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada R2H 2A6

Cardiac sarcolemmal (SL) cis-unsaturated fatty acid sensitive phospholipase D (cis-UFA PLD) is modulated by SL Ca2+-independent phospholipase A2 (iPLA2) activity via intramembrane release of cis-UFA. As PLD-derived phosphatidic acid influences intracellular Ca2+ concentration and contractile performance of the cardiomyocyte, changes in iPLA2 activity may contribute to abnormal function of the failing heart. We examined PLA2 immunoprotein expression and activity in the SL and cytosol from noninfarcted left ventricular (LV) tissue of rats in an overt stage of congestive heart failure (CHF). Hemodynamic assessment of CHF animals showed an increase of the LV end-diastolic pressure with loss of contractile function. In normal hearts, immunoblot analysis revealed the presence of cytosolic PLA2 (cPLA2) and secretory PLA2 (sPLA2) in the cytosol, with cPLA2 and iPLA2 in the SL. Intracellular PLA2 activity was predominantly Ca2+ independent, with minimal sPLA2 activity. CHF increased cPLA2 immunoprotein and PLA2 activity in the cytosol and decreased SL iPLA2 and cPLA2 immunoprotein and SL PLA2 activity. sPLA2 activity and abundance decreased in the cytosol and increased in SL in CHF. The results show that intrinsic to the pathophysiology of post-myocardial infarction CHF are abnormalities of SL PLA2 isoenzymes, suggesting that PLA2-mediated bioprocesses are altered in CHF.

myocardial infarction; signal transduction; phospholipase D

dagger Deceased Nov 24 2000.




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