JBC Invitrogen Ultrasensitive Cytokine Assays

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Originally published In Press as doi:10.1074/jbc.M200475200 on March 1, 2002

J. Biol. Chem., Vol. 277, Issue 19, 16750-16757, May 10, 2002
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Peroxisome Proliferator-activated Receptor (PPAR) gamma  Coactivator-1 Recruitment Regulates PPAR Subtype Specificity*

Hannes OberkoflerDagger , Harald EsterbauerDagger , Veronika LinnemayrDagger , A. Donny Strosberg§, Franz Krempler, and Wolfgang PatschDagger ||

From the Dagger  Department of Laboratory Medicine, Landeskliniken Salzburg, A-5020 Austria, the  Department of Internal Medicine, Krankenhaus Hallein, A-5400 Austria, and the § Institute Cochin de Genetique Moleculaire, Paris, 75014 France

The peroxisome proliferator-activated receptors (PPAR) alpha  and gamma  play key roles in the transcriptional control of contrasting metabolic pathways such as adipogenesis and fatty acid beta -oxidation. Both ligand-activated nuclear receptors bind to common target gene response elements and interact with distinct domains of the transcriptional coactivator PGC-1 to attain their full transcriptional potency. Thus, PPAR subtype specificity may be determined by ligand availability and transcription factor or coactivator expression levels. To identify other, perhaps more precise mechanisms contributing to PPAR subtype specificity, we studied PGC-1 recruitment by PPARs using a previously described hormone response element in the human UCP1 promoter and a human brown adipocyte cell line as our model system. As in rodents, PGC-1 is involved in the transcriptional regulation of the UCP1 gene in humans and mediates the effects of PPARalpha and PPARgamma agonists and retinoic acid. Interestingly, a previously postulated PGC-1 repressor selectively affects the PPARalpha -mediated activation of UCP1 gene expression. Furthermore, inhibition of p38 MAPK signaling, known to regulate the PGC-1/repressor interaction, decreases the stimulatory effect of PPARalpha agonist treatment without reducing the response to thiazolidinedione or retinoic acid. These data support a model whereby PPAR subtype specificity is regulated by recruitment of PGC-1.

* This work was supported by Oesterreichische Nationalbank Project 9364, the Medizinische Forschungsgesellschaft Salzburg, and the Stiftung Propter Homines, Vaduz, Liechtenstein.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Dept. of Laboratory Medicine, Landeskliniken Salzburg, A-5020 Salzburg, Austria. Tel.: 43-662-4482-3800; Fax: 43-662-4482-885; E-mail: w.patsch@lks.at.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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