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Originally published In Press as doi:10.1074/jbc.M003827200 on July 11, 2000

J. Biol. Chem., Vol. 275, Issue 37, 28834-28842, September 15, 2000
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Estrogen Targets Genes Involved in Protein Processing, Calcium Homeostasis, and Wnt Signaling in the Mouse Uterus Independent of Estrogen Receptor-alpha and -beta *

Sanjoy K. DasDagger §, Jian TanDagger , Shefali RajaDagger , Jyotsnabaran Halder§, Bibhash C. Paria§||, and Sudhansu K. Dey§

From the Dagger  Department of Obstetrics & Gynecology, the § Department of Molecular & Integrative Physiology, and the || Department of Pediatrics, Ralph L. Smith Research Center, University of Kansas Medical Center, Kansas City, Kansas 66160

Estrogen actions in target organs are normally mediated via activation of nuclear estrogen receptors (ERs). By using mRNA differential display technique, we show, herein, that estradiol-17beta (E2) and its catechol metabolite 4-hydroxy-E2 (4OHE2) can modulate uterine gene expression in ERalpha (-/-) mice. Whereas administration of E2 or 4OHE2 rapidly up-regulated (4-8-fold) the expression of immunoglobulin heavy chain binding protein (Bip), calpactin I (CalP), calmodulin (CalM), and Sik similar protein (Sik-SP) genes in ovariectomized wild-type or ERalpha (-/-) mice, the expression of secreted frizzled related protein-2 (SFRP-2) gene was down-regulated (4-fold). Bip, CalP, and CalM are calcium-binding proteins and implicated in calcium homeostasis, whereas SFRP-2 is a negative regulator of Wnt signaling. Bip and Sik-SP also possess chaperone-like functions. Administration of ICI-182,780 or cycloheximide failed to influence these estrogenic responses, demonstrating that these effects occur independent of ERalpha , ERbeta , or protein synthesis. In situ hybridization showed differential cell-specific expression of these genes in wild-type and ERalpha (-/-) uteri. Although progesterone can antagonize or synergize estrogen actions, it had minimal effects on these estrogenic responses. Collectively, the results demonstrate that estrogens have a unique ability to influence specific genes in the uterus not involving classical nuclear ERs.

* This work was supported in part by National Institutes of Health Grants ES-07814 (to S. K. Das), HD-12304, and HD-29968 (to S. K. Dey).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.

To whom correspondence should be addressed: Dept. of Obstetrics & Gynecology, MRRC 37/3004, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160-7338. Tel.: 913-588-7379; Fax: 913-588-5677; E-mail: sdas@kumc.edu.

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