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J. Biol. Chem., Vol. 281, Issue 7, 4540-4547, February 17, 2006

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Regulation of Nuclear Translocation of HDAC3 by IB Is Required for Tumor Necrosis Factor Inhibition of Peroxisome Proliferator-activated Receptor Function^*

Zhanguo Gao, Qing He, Bailu Peng, Paul J. Chiao, and Jianping Ye¹

From the Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana 70808 and Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Inhibition of peroxisome proliferator-activated receptor (PPAR) function by TNF- contributes to glucose and fatty acid metabolic disorders in inflammation and cancer, although the molecular mechanism is not fully understood. In this study, we demonstrate that nuclear translocation of HDAC3 is regulated by TNF-, and this event is required for inhibition of transcriptional activity of PPAR by TNF-. HDAC3 is associated with IB in the cytoplasm. After IB degradation in response to TNF-, HDAC3 is subject to nuclear translocation, leading to an increase in HDAC3 activity in the nucleus. This event leads to subcellular redistribution of HDAC3. Knock-out of IB, but not p65 or p50, leads to disappearance of HDAC3 in the cytoplasm, which is associated with HDAC3 enrichment in the nucleus. These data suggest that inhibition of PPAR by TNF- is not associated with a reduction in the DNA binding activity of PPAR. Rather, these results suggest that IB-dependent nuclear translocation of HDAC3 is responsible for PPAR inhibition by TNF-.

Received for publication, July 18, 2005 , and in revised form, December 16, 2005.

^* This study is supported by National Institutes of Health Grant DK068036 and an American Diabetes Association research award (to J. Y.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Pennington Biomedical Research Center, 6400 Perkins Rd., Baton Rouge, LA 70808. Tel.: 225-763-3163; Fax: 225-763-2525; E-mail: yej{at}pbrc.edu.

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