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Am J Physiol Endocrinol Metab (November 4, 2003). doi:10.1152/ajpendo.00392.2003
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Submitted on August 29, 2003
Accepted on October 24, 2003

PPAR-{gamma} is not required for the inhibitory actions of 15-deoxy {Delta} 12, 14-Prostaglandin J2 on cytokine signaling in pancreatic {beta}-cells

Sarah M. Weber1, Anna L. Scarim1, and John A. Corbett1*

1 Edward A. Doisy Department of Biochemistry and Molecular Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: corbettj{at}slu.edu.

PPAR-{gamma} agonists such as 15-deoxy {Delta}12, 14 Prostaglandin J (PGJ2) and troglitazone have been shown to elicit anti-inflammatory effects in pancreatic {beta}-cells that include inhibition of cytokine-stimulated iNOS gene expression and production of nitric oxide. In addition, these ligands impair IL-1-induced NF-{kappa}B and MAPK as well as IFN-{gamma}-stimulated STAT-1 activation in {beta}-cells. The purpose of this study was to determine if PPAR-{gamma} activation participates in the anti-inflammatory actions of PGJ2 in {beta}-cells. Pretreatment of RINm5F cells for 6 h with PGJ2 results in inhibition of IL-1 stimulated I{kappa}B degradation and IFN-{gamma} stimulated STAT-1 phosphorylation. Overexpression of a dnPPAR-{gamma} mutant or treatment with the PPAR-{gamma} antagonist GW9662 does not modulate the inhibitory actions of PGJ2 on cytokine signaling in RINm5F cells. While these agents fail to attenuate the inhibitory actions of PGJ2 on cytokine signaling, they do inhibit PGJ2- stimulated PPRE reporter activity. Consistent with the inability to attenuate the inhibitory actions of PGJ2 on cytokine signaling, neither dnPPAR-{gamma} nor GW9662 prevent the inhibitory actions of PGJ2 on IL-1-stimulated iNOS gene expression or nitric oxide production by RINm5F cells. These findings support a PPAR-{gamma}-independent mechanism by which PPAR-{gamma} ligands impair cytokine signaling and iNOS expression by islets.




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