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Cardiovascular Research Advance Access [Accepted Manuscript] published online on January 8, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp004
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Angiotensin II downregulates the fatty acid oxidation pathway in adult rat cardiomyocytes via release of tumor necrosis factor-{alpha}

Corinne Pellieux, Christophe Montessuit, Irène Papageorgiou and René Lerch

Cardiology Center, Department of Medicine, University Hospitals of Geneva, Foundation for Medical Research, Geneva 4, Switzerland

Correspondence to: Corinne Pellieux, Ph.D., Cardiology Center, Department of Medicine, University Hospitals of Geneva, Foundation for Medical Research, 64, avenue de la Roseraie, CH-1211 Geneva 4, Switzerland, Phone :+41 22 372 72 22, Fax: +41 22 372 72 29, E-mail: corinne.pellieux{at}hcuge.ch

Aim: Advanced heart failure is often associated with reduced myocardial fatty acid oxidation capacity. We have previously observed that failing hearts of mice with overexpression of angiotensinogen in the myocardium exhibit marked reduction of key regulatory proteins of fatty acid oxidation. In the present study we determined whether exposure of adult rat cardiac myocytes to angiotensin II (Ang II) influences expression of fatty acid translocase, muscle-type carnitine palmitoyl transferase-I and medium-chain acyl-CoA dehydrogenase.

Methods and results: Ang II reduced mRNA expression of the three regulatory proteins in adult rat cardiac myocytes during the entire 14-days culture period. However protein expression and palmitate oxidation rate remained unaltered for 7 days, but subsequently markedly decreased. The decrease of protein expression and of fatty acid oxidation coincided with the onset of increased protein expression of tumor necrosis factor-{alpha} (TNF-{alpha}). The effect of Ang II was completely abolished by either blocking TNF-{alpha} formation through inhibition of reactive oxygen species-mediated activation of nuclear factor-{kappa}B or by neutralizing TNF-{alpha} with a specific antibody. Activation of peroxisome proliferator-activated receptor-{alpha} (PPAR{alpha}) and PPARβ/{delta} counteracted Ang IImediated reduction of the fatty acid oxidation pathway.

Conclusion: Prolonged exposure of cardiac myocytes to Ang II elicits downregulation of the fatty acid oxidation pathway mediated by enhanced synthesis of TNF-{alpha}.

KEYWORDS myocytes; cell culture; energy metabolism; angiotensin; remodeling

Time for primary review: 26 Days


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