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(The FASEB Journal. 2001;15:833-845.)
© 2001 FASEB

Uncoupling protein 3 transcription is regulated by peroxisome proliferator-activated receptor {alpha} in the adult rodent heart

MARTIN E. YOUNG, SARITA PATIL, JUN YING, CHRISTOPHE DEPRE, HARLEEN SINGH AHUJA*, GREGORY L. SHIPLEY*, STANISLAW M. STEPKOWSKI{dagger}, PETER J. A. DAVIES* and HEINRICH TAEGTMEYER1

Division of Cardiology,
* Department of Integrative Biology, and the
{dagger} Division of Organ Transplantation, University of Texas Houston Medical Center, Houston, Texas 77030, USA

1Correspondence: Division of Cardiology,, University of Texas Houston Medical School, 6431 Fannin, MSB 1.246, Houston, TX 77030, USA. E-mail: ht{at}heart.med.uth.tmc.edu

Relatively little is known concerning the regulation of uncoupling proteins (UCPs) in the heart. We investigated in the adult rodent heart 1) whether changes in workload, substrate supply, or cytokine (TNF-{alpha}) administration affect UCP-2 and UCP-3 expression, and 2) whether peroxisome proliferator-activated receptor {alpha} (PPAR{alpha}) regulates the expression of either UCP-2 or UCP-3. Direct comparisons were made between cardiac and skeletal muscle. UCP-2, UCP-3, and PPAR{alpha} expression were reduced when cardiac workload was either increased (pressure overload by aortic constriction) or decreased (mechanical unloading by heterotopic transplantation). Similar results were observed during cytokine administration. Reduced dietary fatty acid availability resulted in decreased expression of both cardiac UCP-2 and UCP-3. However, when fatty acid (the natural ligand for PPAR{alpha}) supply was increased (high-fat feeding, fasting, and STZ-induced diabetes), cardiac UCP-3 but not UCP-2 expression increased. Comparable results were observed in rats treated with the specific PPAR{alpha} agonist WY-14,643. The level of cardiac UCP-3 but not UCP-2 expression was severely reduced (20-fold) in PPAR{alpha}-/- mice compared to wild-type mice. These results suggest that in the adult rodent heart, UCP-3 expression is regulated by PPAR{alpha}. In contrast, cardiac UCP-2 expression is regulated in part by a fatty acid-dependent, PPAR{alpha}-independent mechanism.—Young, M. E., Patil, S., Ying, J., Depre, C., Ahuja, H. S., Shipley, G. L., Stepkowski, S. M., Davies, P. J. A., Taegtmeyer H. Uncoupling protein 3 transcription is regulated by peroxisome proliferator-activated receptor {alpha} in the adult rodent heart.


Key Words: diabetes • fasting • fatty acids • hypertrophy • unloading




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