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Originally published In Press as doi:10.1074/jbc.M205355200 on September 16, 2002

J. Biol. Chem., Vol. 277, Issue 47, 44772-44777, November 22, 2002
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Estradiol Represses Human T-cell Leukemia Virus Type 1 Tax Activation of Tumor Necrosis Factor-alpha Gene Transcription*

Christina Tzagarakis-FosterDagger , Romas Geleziunas§, Abderrahim LomriDagger , Jinping AnDagger , and Dale C. LeitmanDagger ||

From the Dagger  Department of Obstetrics, Gynecology and Reproductive Sciences, Center for Reproductive Sciences, University of California, San Francisco, San Francisco, California 94143 and § Merck Research Laboratories, West Point, Pennsylvania 19486

Adult T-cell leukemia is caused by human T-cell leukemia virus type I (HTLV-I). The HTLV-I Tax protein is essential for clinical manifestations because it activates viral and cellular gene transcription. Tax enhances production of tumor necrosis factor-alpha (TNF-alpha ), which may lead to bone and joint destruction. Because estrogens might prevent osteoporosis by repressing TNF-alpha gene transcription, we investigated whether estrogens inhibit the transcriptional effects of Tax on the TNF-alpha promoter. Tax activated the -1044, -163, and -125 TNF-alpha promoters by 9-25-fold but not the -82 promoter, demonstrating that Tax activation requires the -125 to -82 region, known as the TNF response element (TNF-RE). Three copies of the TNF-RE upstream of the minimal thymidine kinase promoter conferred a similar magnitude of activation by Tax. We demonstrated that c-Jun, NFkappa B, p50, and p65 interact with and activate the TNF-RE by using mutational analysis of the TNF-RE, Tax mutants that selectively activate NFkappa B or the cAMP-response element binding protein/activating transcription factor pathway, and gel shift assays with nuclear extracts. Estradiol markedly repressed Tax-activated transcription of the TNF-alpha gene with estrogen receptor (ER) alpha  or beta . Nuclear extracts from U2OS cells stably transfected with ERalpha demonstrated that ERs interact with the TNF-RE. Our studies provide evidence that ERs repress Tax-activated TNF-alpha transcription by interacting with a c-Jun and NFkappa B platform on the TNF-RE. Estrogens may ameliorate bone and inflammatory joint diseases in patients infected with HTLV-I by repressing transcription of the TNF-alpha gene.

* This work was supported by a National Institutes of Health postdoctoral training grant and a Bank of America Giannini postdoctoral fellowship (to C. T.-F.) and grants from the Paul Beeson Physician Faculty Scholars in Aging Research Program (funded by the Alliance for Aging Research, the John A. Hartford Foundation, the Commonwealth Fund, and the Starr Foundation), the NICHD National Institutes of Health Women's Reproductive Health Research Program, and the Susan B. Komen Foundation (to D. C. L.).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.

Present address: Hop Lariboisiere, INSERM, U349, F-75475 Paris, France.

|| To whom correspondence should be addressed: University of California, San Francisco, Center for Reproductive Sciences, HSE 1619 P.O. Box 0556, San Francisco, CA 94143-0556. Tel.: 415-502-5261; Fax: 415-753-3271; E-mail: leitmand@obgyn.ucsf.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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