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Am J Physiol Heart Circ Physiol 291: H161-H166, 2006. First published February 3, 2006; doi:10.1152/ajpheart.01065.2004
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Deletion of peroxisome proliferator-activated receptor-{alpha} induces an alteration of cardiac functions

Cécile Loichot,1 Laurence Jesel,1 Angela Tesse,1 Antonia Tabernero,1 Kristina Schoonjans,2 Gérard Roul,1 Irina Carpusca,1 Johan Auwerx,2,3 and Ramaroson Andriantsitohaina1

1Laboratoire de Pharmacologie et Physicochimie des Interactions Cellulaires et Moléculaires, UMR-Centre National de la Recherche Scientifique (CNRS) 7034, Faculté de Pharmacie, Université Louis Pasteur (ULP), Illkirch, France, 2Institut de Génétique et Biologie Moléculaire et Cellulaire, CNRS, Institut National de la Santé et de la Recherche Médicale, ULP; and 3Institut Clinique de la Souris, Illkirch, France

Submitted 18 October 2004 ; accepted in final form 30 January 2006

The peroxisome proliferator-activated receptor-{alpha} (PPAR{alpha}) plays a major role in the control of cardiac energy metabolism. The role of PPAR{alpha} on cardiac functions was evaluated by using PPAR{alpha} knockout (PPAR{alpha} –/–) mice. Hemodynamic parameters by sphygmomanometric measurements show that deletion of PPAR{alpha} did not affect systolic blood pressure and heart rate. Echocardiographic measurements demonstrated reduced systolic performance as shown by the decrease of left ventricular fractional shortening in PPAR{alpha} –/– mice. Telemetric electrocardiography revealed neither atrio- nor intraventricular conduction defects in PPAR{alpha} –/– mice. Also, heart rate, P-wave duration and amplitude, and QT interval were not affected. However, the amplitude of T wave from PPAR{alpha} –/– mice was lower compared with wild-type (PPAR{alpha} +/+) mice. When the myocardial function was measured by ex vivo Langendorff's heart preparation, basal and beta-adrenergic agonist-induced developed forces were significantly reduced in PPAR{alpha}-null mice. In addition, Western blot analysis shows that the protein expression of beta1-adrenergic receptor is reduced in hearts from PPAR{alpha} –/– mice. Histological analysis showed that hearts from PPAR{alpha} –/– but not PPAR{alpha} +/+ mice displayed myocardial fibrosis. These results suggest that PPAR{alpha}-null mice have an alteration of cardiac contractile performance under basal and under stimulation of beta1-adrenergic receptors. These effects are associated with myocardial fibrosis. The data shed light on the role of PPAR{alpha} in maintaining cardiac functions.

cardiomyopathy; peroxisome proliferator-activated receptor-{alpha}; cardiac beta1-adrenergic receptor protein expression


Address for reprint requests and other correspondence: R. Andriantsitohaina, Biologie Neuro-Vasculaire Intégrée, UMR-CNRS 6214, INSERM 771, Faculté de Médecine, Université d'Angers, 49045 Angers Cedex, France (ramaroson.andriantsitohaina{at}univ-angers.fr)




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