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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M800561-JLR200 on November 10, 2008

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Journal of Lipid Research, Vol. 50, 1600-1608, August 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Cardiolipin biosynthesis and remodeling enzymes are altered during development of heart failure

Harjot K. Saini-Chohan1,*, Michael G. Holmes1,{dagger}, Adam J. Chicco§, William A. Taylor1, Russell L. Moore**, Sylvia A. McCune**, Diane L. Hickson-Bick{dagger}, Grant M. Hatch2,{dagger} and Genevieve C. Sparagna**

* Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada
{dagger} Department of Pathology and Laboratory Medicine, University of Texas Medical School, Houston, TX
§ Department of Health and Exercise Science, Colorado State University, Fort Collins, CO
** Department of Integrative Physiology, University of Colorado, Boulder, CO

2 To whom correspondence should be addressed. e-mail: hatchgm{at}ms.umanitoba.ca

Cardiolipin (CL) is responsible for modulation of activities of various enzymes involved in oxidative phosphorylation. Although energy production decreases in heart failure (HF), regulation of cardiolipin during HF development is unknown. Enzymes involved in cardiac cardiolipin synthesis and remodeling were studied in spontaneously hypertensive HF (SHHF) rats, explanted hearts from human HF patients, and nonfailing Sprague Dawley (SD) rats. The biosynthetic enzymes cytidinediphosphatediacylglycerol synthetase (CDS), phosphatidylglycerolphosphate synthase (PGPS) and cardiolipin synthase (CLS) were investigated. Mitochondrial CDS activity and CDS-1 mRNA increased in HF whereas CDS-2 mRNA in SHHF and humans, not in SD rats, decreased. PGPS activity, but not mRNA, increased in SHHF. CLS activity and mRNA decreased in SHHF, but mRNA was not significantly altered in humans. Cardiolipin remodeling enzymes, monolysocardiolipin acyltransferase (MLCL AT) and tafazzin, showed variable changes during HF. MLCL AT activity increased in SHHF. Tafazzin mRNA decreased in SHHF and human HF, but not in SD rats. The gene expression of acyl-CoA: lysocardiolipin acyltransferase-1, an endoplasmic reticulum MLCL AT, remained unaltered in SHHF rats. The results provide mechanisms whereby both cardiolipin biosynthesis and remodeling are altered during HF. Increases in CDS-1, PGPS, and MLCL AT suggest compensatory mechanisms during the development of HF. Human and SD data imply that similar trends may occur in human HF, but not during nonpathological aging, consistent with previous cardiolipin studies.

Supplementary key words acyl-Coenzyme A:lysocardiolipin acyltransferase-1 • cardiolipin synthase • cytidinediphosphate-diacylglycerol synthetase • human heart failure • monolysocardiolipin acyltransferase • phosphatidylglycerol phosphate synthase • phospholipid enzyme • spontaneously hypertensive heart failure rat • tafazzin

Abbreviations: CDS, cytidinediphosphatediacylglycerol synthetase; CL, cardiolipin; CLS, cardiolipin synthase; HF, heart failure; MLCL AT, monolysocardiolipin acyltransferase; PGPS, phosphatidylglycerolphosphate synthase; SD, Sprague Dawley; SHHF, spontaneously hypertensive heart failure; TAZ, tafazzin


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