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J. Lipid Res.
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A more recent version of this article appeared on November 1, 2004

Papers In Press, published online ahead of print August 16, 2004
J. Lipid Res., doi:10.1194/jlr.M400049-JLR200
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Submitted on February 9, 2004
Revised on July 27, 2004
Accepted on August 15, 2004

Rosiglitazone upregulates caveolin-1 expression in THP-1 cells through a PPAR-dependent mechanism

Gemma Llaverias, Manuel Vázquez-Carrera, Rosa M. Sánchez, Véronique Noé, Carlos J. Ciudad, Juan C. Laguna, and Marta Alegret

Department of Pharmacology, University of Barcelona, School of Pharmacy, Barcelona, Barcelona 08028

Corresponding Author: alegret{at}ub.edu

Peroxisome proliferator-activated receptor g (PPARg) activation or overexpression induce caveolin-1 expression in several cell types. The objective of this study was to investigate if PPAR agonists could also regulate the caveolin-1 gene in macrophages, and to explore the mechanisms involved. Our experiments demonstrated that rosiglitazone dose- and time-dependently increased caveolin-1 mRNA and protein in THP-1 macrophages. This induction was not observed in the presence of inhibitors of transcription or de novo protein synthesis. We also showed that the increase in caveolin-1 elicited by rosiglitazone was not related either to macrophage differentiation or to cellular apoptosis. The inductive effect seems to be dependent on PPAR activation, as the PPAR antagonist GW9662 abolished it. The activation of the liver X receptor (LXR) with 22(R)-hydroxycholesterol also increased caveolin-1 mRNA, while the inactive (S) isomer did not. Finally, we identified a functional peroxisome proliferator response element (PPRE) in the caveolin-1 promoter, which was activated upon rosiglitazone treatment in THP-1 macrophages.


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