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Originally published In Press as doi:10.1074/jbc.M001286200 on July 21, 2000

J. Biol. Chem., Vol. 275, Issue 39, 30232-30239, September 29, 2000
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C/EBP Regulates Hepatic Transcription of 11beta -Hydroxysteroid Dehydrogenase Type 1
A NOVEL MECHANISM FOR CROSS-TALK BETWEEN THE C/EBP AND GLUCOCORTICOID SIGNALING PATHWAYS*

Louise J. S. WilliamsDagger §, Val LyonsDagger , Iolaina MacLeodDagger , Vidya RajanDagger , Gretchen J. Darlington, Valeria Poli||, Jonathan R. SecklDagger , and Karen E. ChapmanDagger **

From the Dagger  Molecular Endocrinology group, University of Edinburgh, Molecular Medicine Centre, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom, the  Huffington Center on Aging, N805, Baylor College of Medicine, Houston, Texas 77030, and the || Department of Biochemistry, University of Dundee, Dundee DD1 4HN, United Kingdom

Glucocorticoid action within individual cells is potently modulated by 11beta -hydroxysteroid dehydrogenase (11beta -HSD), which, by interconverting active and inert glucocorticoids, determines steroid access to receptors. Type 1 11beta -HSD (11beta -HSD1) is highly expressed in liver where it regenerates glucocorticoids, thus amplifying their action and contributing to induction of glucocorticoid-responsive genes, most of which are also regulated by members of the C/EBP (CAAT/enhancer-binding protein) family of transcription factors. Here we demonstrate that C/EBPalpha is a potent activator of the 11beta -HSD1 gene in hepatoma cells and that mice deficient in C/EBPalpha have reduced hepatic 11beta -HSD1 expression. In contrast, C/EBPbeta is a relatively weak activator of 11beta -HSD1 transcription in hepatoma cells and attenuates C/EBPalpha induction, and mice that lack C/EBPbeta have increased hepatic 11beta -HSD1 mRNA. The 11beta -HSD1 promoter (between -812 and +76) contains 10 C/EBP binding sites, and mutation of the promoter proximal sites decreases the C/EBP inducibility of the promoter. One site encompasses the transcription start, and both C/EBPalpha and C/EBPbeta are present in complexes formed by liver nuclear proteins at this site. The regulation of 11beta -HSD1 expression, and hence intracellular glucocorticoid levels, by members of the C/EBP family provides a novel mechanism for cross-talk between the C/EBP family of transcription factors and the glucocorticoid signaling pathway.

* This work was supported by a Medical Research Council project grant (to K. E. C. and J. R. S.), a Wellcome Trust program grant, and a Wellcome Senior Clinical Research Fellowship (to J. R. S.).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.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) Y10420.

§ Current address, Endocrine Unit, Massachusetts General Hospital, BUL-327, Boston, MA 02114.

** To whom correspondence should be addressed: Tel.: 44-131-651-1033; Fax: 44-131-651-1085; E-mail: karen.chapman@ed.ac.uk.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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