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First published on January 31, 2005; DOI: 10.1124/mol.104.004895

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Received for publication July 13, 2004.
Revised January 31, 2005.
Accepted for publication January 31, 2005.

Mechanism of the anti-inflammatory effect of thiazolidindiones. Relationship with the glucocorticoid pathway

Armando Ialenti 1, Gianluca Grassia 1, Paola Di Meglio 1, Pasquale Maffia 1, Massimo Di Rosa 1, Angela Ianaro 1*

1 Department of Experimental Pharmacology University of Naples Federico II

* Address correspondence to: E-mail: ianaro{at}unina.it

Abstract

The glucocorticoid receptor (GR) and peroxisome proliferators-activated receptors (PPARs) play important roles in both physiological and pathological conditions such as cell differentiation, lipolisis, control of glucose metabolism, immunity and inflammation. In fact, recent studies suggest that the thiazolidindiones (TZDs) class of PPAR-{gamma} ligands, like glucocorticoids, may also be clinically beneficial in several inflammatory diseases, even if the molecular mechanisms responsible for these activities have not yet been clarified. In this study, by using a murine model of inflammation, the carrageenin-induced paw edema in mouse, we show that the anti-inflammatory activity exhibited by the PPAR-{gamma} agonists rosiglitazone and ciglitazone is reverted by the GR antagonist RU486. Moreover, by using a conditional GR null cell line, we demonstrate, for the first time to our knowledge, that one of the possible mechanisms explaining TZDs anti-inflammatory activity could be their ability to activate GR nuclear translocation. In addition, by using J774 cell line lacking PPAR-{gamma}, we demonstrate that PPAR-{gamma} expression could not be essential for TZDs-mediated GR nuclear translocation, thus explaining, at least in part, the molecular mechanism underlying their anti-inflammatory activity.


Key words: Glucorticoids/Mineralocorticoids, PPARs


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