J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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Originally published In Press as doi:10.1194/jlr.M600551-JLR200 on April 10, 2007

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Journal of Lipid Research, Vol. 48, 1559-1570, July 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Loss of cardiac tetralinoleoyl cardiolipin in human and experimental heart failure

Genevieve C. Sparagna1,2,*, Adam J. Chicco1,*, Robert C. Murphy{dagger}, Michael R. Bristow§, Christopher A. Johnson{dagger}, Meredith L. Rees*, Melissa L. Maxey*, Sylvia A. McCune* and Russell L. Moore*

* Department of Integrative Physiology, University of Colorado Cardiovascular Institute, University of Colorado at Boulder, Boulder, CO 80309-0354
{dagger} Department of Pharmacology, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045-0511
§ Division of Cardiology, University of Colorado Health Sciences Center, Denver, CO 80262

Published, JLR Papers in Press, April 10, 2007.

1 G. C. Sparagna and A. J. Chicco contributed equally to this work.

2 To whom correspondence should be addressed. e-mail: sparagna{at}colorado.edu

The mitochondrial phospholipid cardiolipin is required for optimal mitochondrial respiration. In this study, cardiolipin molecular species and cytochrome oxidase (COx) activity were studied in interfibrillar (IF) and subsarcolemmal (SSL) cardiac mitochondria from Spontaneously Hypertensive Heart Failure (SHHF) and Sprague-Dawley (SD) rats throughout their natural life span. Fisher Brown Norway (FBN) and young aortic-constricted SHHF rats were also studied to investigate cardiolipin alterations in aging versus pathology. Additionally, cardiolipin was analyzed in human hearts explanted from patients with dilated cardiomyopathy. A loss of tetralinoleoyl cardiolipin (L4CL), the predominant species in the healthy mammalian heart, occurred during the natural or accelerated development of heart failure in SHHF rats and humans. L4CL decreases correlated with reduced COx activity (no decrease in protein levels) in SHHF cardiac mitochondria, but with no change in citrate synthase (a matrix enzyme) activity. The fraction of cardiac cardiolipin containing L4CL became much lower with age in SHHF than in SD or FBN mitochondria. In summary, a progressive loss of cardiac L4CL, possibly attributable to decreased remodeling, occurs in response to chronic cardiac overload, but not aging alone, in both IF and SSL mitochondria. This may contribute to mitochondrial respiratory dysfunction during the pathogenesis of heart failure.

Supplementary key words phospholipids • mitochondria • linoleic acid • cytochrome oxidase • congestive heart failure • cardiomyopathy • aging


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