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Originally published In Press as doi:10.1074/jbc.M009284200 on December 12, 2000

J. Biol. Chem., Vol. 276, Issue 12, 9016-9027, March 23, 2001
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Interleukin-6-induced Tethering of STAT3 to the LAP/C/EBPbeta Promoter Suggests a New Mechanism of Transcriptional Regulation by STAT3*

Monika NiehofDagger §, Konrad StreetzDagger , Tim RakemannDagger , Stephan C. BischoffDagger , Michael P. MannsDagger , Friedemann Horn||, and Christian TrautweinDagger **

From the Dagger  Department of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, 30625 Hannover and the || Institute of Clinical Immunology, Universität Leipzig, 04129 Leipzig, Germany

LAP/C/EBPbeta is a member of the C/EBP family of transcription factors and contributes to the regulation of the acute phase response in hepatocytes. Here we show that IL-6 controls LAP/C/EBPbeta gene transcription and identify an IL-6 responsive element in the LAP/C/EBPbeta promoter, which contains no STAT3 DNA binding motif. However, luciferase reporter gene assays showed that STAT3 activation through the gp130 signal transducer molecule is involved in mediating IL-6-dependent LAP/C/EBPbeta transcription. Southwestern analysis indicated that IL-6 induces binding of a 68-kDa protein to the recently characterized CRE-like elements in the LAP/C/EBPbeta promoter. Transfection experiments using promoter constructs with mutated CRE-like elements revealed that these sites confer IL-6 responsiveness. Further analysis using STAT1/STAT3 chimeras identified specific domains of the protein that are required for the IL-6-dependent increase in LAP/C/EBPbeta gene transcription. Overexpression of the amino-terminal domain of STAT3 blocked the IL-6-mediated response, suggesting that the STAT3 amino terminus has an important function in IL-6-mediated transcription of the LAP/C/EBPbeta gene. These data lead to a model of how tethering STAT3 to a DNA-bound complex contributes to IL-6-dependent LAP/C/EBPbeta gene transcription. Our analysis describes a new mechanism by which STAT3 controls gene transcription and which has direct implication for the acute phase response in liver cells.

* This work was supported by the Sonderforschungsbereich 566, project B08.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

This work is dedicated on the occasion of Prof. Dr. W. Gerok's 75th birthday.

§ Present address: Fraunhofer-Institut, D-30625 Hannover, Germany.

Present address: Dianova, D-20354 Hamburg, Germany.

** To whom correspondence should be addressed: Dept. of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. Tel.: 49-511-532-3489; Fax: 49-511-532-4896; E-mail: trautwein.christian@mh-hannover.de.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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