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Cardiovascular Research Advance Access [Corrected Proof] published online on August 18, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn184
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
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Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation

Mariana G. Rosca1, Edwin J. Vazquez1,2, Janos Kerner3, William Parland1, Margaret P. Chandler4, William Stanley5, Hani N. Sabbah6 and Charles L. Hoppel1,2,*

1 Department of Medicine, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland 44106-4981, OH, USA
2 Department of Pharmacology, Case Western Reserve University, Cleveland, OH, USA
3 Department of Nutrition, Case Western Reserve University, Cleveland, OH, USA
4 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
5 Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, Baltimore, MD, USA
6 Department of Medicine, Henry Ford Hospital, Henry Ford Heart and Vascular Institute, Detroit, MI, USA

* Corresponding author. Tel: +1 216 368 3147; fax: +1 216 368 5162. E-mail address: charles.hoppel{at}case.edu

Aims: Mitochondrial dysfunction is a major factor in heart failure (HF). A pronounced variability of mitochondrial electron transport chain (ETC) defects is reported to occur in severe acquired cardiomyopathies without a consistent trend for depressed activity or expression. The aim of this study was to define the defect in the integrative function of cardiac mitochondria in coronary microembolization-induced HF.

Methods and results: Studies were performed in the canine coronary microembolization-induced HF model of moderate severity. Oxidative phosphorylation was assessed as the integrative function of mitochondria, using a comprehensive variety of substrates in order to investigate mitochondrial membrane transport, dehydrogenase activity and electron-transport coupled to ATP synthesis. The supramolecular organization of the mitochondrial ETC also was investigated by native gel electrophoresis. We found a dramatic decrease in ADP-stimulated respiration that was not relieved by an uncoupler. Moreover, the ADP/O ratio was normal, indicating no defect in the phosphorylation apparatus. The data point to a defect in oxidative phosphorylation within the ETC. However, the individual activities of ETC complexes were normal. The amount of the supercomplex consisting of complex I/complex III dimer/complex IV, the major form of respirasome considered essential for oxidative phosphorylation, was decreased.

Conclusions: We propose that the mitochondrial defect lies in the supermolecular assembly rather than in the individual components of the ETC.

KEYWORDS Heart failure; Mitochondria; Oxidative phosphorylation; Respirasomes; Electron transport chain complexes

Time for primary review: 19 days


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