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Papers In Press, published online ahead of print January 23, 2001
J. Biol. Chem, 10.1074/jbc.M007237200
Submitted on August 9, 2000
Revised on January 22, 2001
Accepted on January 22, 2001

PPARg ligands suppress the transcriptional activation of cyclooxygenase-2. Evidence for involvement of AP-1 and CBP/p300

Kotha Subbaramaiah, Derrick T. Lin, Janice C. Hart, and Andrew J. Dannenberg

Medicine, Weill Medical College of Cornell University, Newe York, NY 10021

Corresponding Author: ksubba{at}pop.med.cornell.edu

We investigated whether PPARg ligands (ciglitazone, troglitazone, 15d-PGJ2) inhibited COX-2 induction in human epithelial cells. Ligands of PPARg inhibited phorbol ester (PMA)-mediated induction of COX-2 and PGE2 synthesis. Nuclear run-offs revealed increased rates of COX-2 transcription after treatment with PMA, an effect that was inhibited by PPARg ligands. PMA-mediated induction of COX-2 promoter activity was inhibited by PPARg ligands; this suppressive effect was prevented by overexpressing a dominant negative form of PPARg or a PPRE decoy oligonucleotide. The stimulatory effects of PMA were mediated by a cyclic AMP response element (CRE) in the COX-2 promoter. Treatment with PMA increased activator protein-1 (AP-1) activity and the binding of c-Jun, c-Fos and ATF-2 to the CRE, effects that were blocked by PPARg ligands. These findings raised questions about the mechanism underlying the anti-AP-1 effect of PPARg ligands. The induction of c-Jun by PMA was blocked by PPARg ligands. Overexpression of either c-Jun or CREB-binding protein (CBP)/p300 partially relieved the suppressive effect of PPARg ligands. When CBP and c-Jun were overexpressed together, the ability of PPARg ligands to suppress PMA-mediated induction of COX-2 promoter activity was essentially abrogated. Bisphenol A diglycidyl ether, a compound which binds to PPARg but lacks the ability to activate transcription, also inhibited PMA-mediated induction of AP-1 activity and COX-2. Taken together, these findings are likely to be important for understanding the anti-inflammatory and anti-cancer properties of PPARg ligands.


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