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Endocrinology Vol. 143, No. 7 2559-2570
Copyright © 2002 by The Endocrine Society

RECEPTORS

Estrogen Receptor {alpha} Inhibits IL-1ß Induction of Gene Expression in the Mouse Liver

Mark J. Evans, Kehdih Lai, Lucinda J. Shaw, Douglas C. Harnish and Christopher C. Chadwick

Wyeth Research, Collegeville, Pennsylvania 19426

Address all correspondence and requests for reprints to: Dr. Mark Evans, Wyeth Research, 500 Arcola Road, Collegeville, Pennsylvania 19426. E-mail: . evansm{at}wyeth.com

Estrogens have been suggested to modulate several inflammatory processes. Here, we show that IL-1ß treatment induced the expression of approximately 75 genes in the liver of ovariectomized mice. 17{alpha}-Ethinyl estradiol (EE) pretreatment reduced the IL-1ß induction of approximately one third of these genes. Estrogen receptor {alpha} (ER{alpha}) was required for this inhibitory activity, because EE inhibition of IL-1ß-stimulated gene expression occurred in ERß knockout mice, but not in ER{alpha} knockout mice. EE treatment induced expression of 40 genes, including the transcriptional repressor short heterodimer partner and prostaglandin D synthase, known modulators of nuclear factor-{kappa}B signaling. However, the ER agonists genistein and raloxifene both inhibited IL-1ß gene induction without stimulating the expression of prostaglandin D synthase, short heterodimer partner, or other ER-inducible genes, indicating that induction of gene expression was not required for ER inhibition of IL-1ß signaling. Finally, the ability of EE to repress IL-1ß gene induction varied among tissues. For example, EE inhibited IL-1ß induction of lipopolysaccharide-induced c-x-c chemokine (LIX) in the liver, but not in the spleen or lung. The degree of EE repression did not correlate with ER expression. cAMP response element binding protein-binding protein (CBP)/p300 levels also varied between tissues. Together, these results are consistent with a model of in vivo ER interference with IL-1ß signaling through a coactivator-based mechanism.




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