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The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 10 4667-4672
Copyright © 2002 by The Endocrine Society

Original Article

Regulation of Proinflammatory Cytokines in Human Gestational Tissues by Peroxisome Proliferator-Activated Receptor-{gamma}: Effect of 15-Deoxy-{Delta}12,14-PGJ2 and Troglitazone

Martha Lappas, Michael Permezel, Harry M. Georgiou and Gregory E. Rice

Department of Obstetrics and Gynaecology, University of Melbourne, Mercy Perinatal Research Centre, Mercy Hospital for Women, East Melbourne, Victoria, Australia 3002

Address all correspondence and requests for reprints to: Martha Lappas, M.D., Department of Obstetrics and Gynecology, University of Melbourne, Mercy Hospital for Women, 126 Clarendon Street, East Melbourne 3002, Victoria, Australia. E-mail: mlappas{at}unimelb.edu.au.

Abstract

Peroxisome proliferator-activated receptor (PPAR)-{gamma} is a ligand-dependent nuclear receptor that is essential for murine placental development and trophoblast differentiation. In nonreproductive tissues, PPAR-{gamma} regulates the formation of proinflammatory cytokines. Evidence suggests that many of the observed anti-inflammatory effects of PPAR-{gamma} are in part caused by antagonizing the activities of the transcription factors, including nuclear factor-{kappa}B. The aim of this study was to elucidate whether natural [15-deoxy-{Delta}12,14-PGJ2 (15d-PGJ2)] and synthetic (troglitazone) PPAR-{gamma} ligands regulate the secretion of IL-6, IL-8, and TNF-{alpha} from human intrauterine tissues. Human placenta, amnion, and choriodecidual tissues were incubated in the presence of 10 µg/ml lipopolysaccharide in the absence (control) or presence of 30 µM 15d-PGJ2 (n = 6 independent placenta) or troglitazone (n = 6 independent placentas). After a 6-h incubation, the incubation medium was collected and the release of IL-6, IL-8, and TNF-{alpha} was quantified by ELISA. Treatment of placental, amnion, and choriodecidual tissues with both 15d-PGJ2 and troglitazone significantly reduced the release of lipopolysaccharide-stimulated IL-6, IL-8, and TNF-{alpha} (t test, P < 0.05). Gel shift analyses demonstrated that 15d-PGJ2, but not troglitazone, suppressed nuclear factor-{kappa}B DNA-binding activity. The data presented in this study demonstrate that the formation of proinflammatory mediators can be modulated by currently available therapeutic agents and may therefore be of therapeutic potential in human labor.




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