Chinyu G. Su, Xiaoming Wen, Shannon T. Bailey, Wen Jiang, Shamina M. Rangwala, Sue A. Keilbaugh, Anne Flanigan, Sreekant Murthy, Mitchell A. Lazar, Gary D. Wu
J Clin Invest.
1999;
104(4):383–389
doi:10.1172/JCI7145
This article Copyright © 1999, The American Society for Clinical Investigation
Abstract
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P
eroxisome proliferator-activated receptor γ (PPAR-γ), a member of the nuclear hormone receptor superfamily originally shown to play a critical role in adipocyte differentiation and glucose homeostasis, has recently been implicated as a regulator of cellular proliferation and inflammatory responses. Colonic epithelial cells, which express high levels of PPAR-γ protein, have the ability to produce inflammatory cytokines that may play a role in inflammatory bowel disease (IBD). We report here that PPAR-γ ligands dramatically attenuate cytokine gene expression in colon cancer cell lines by inhibiting the activation of nuclear factor-κB via an IκB-α–dependent mechanism. Moreover, thiazolidinedione ligands for PPAR-γ markedly reduce colonic inflammation in a mouse model of IBD. These results suggest that colonic PPAR-γ may be a therapeutic target in humans suffering from IBD.J. Clin. Invest. 104:383-389(1999).
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