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Endocrinology Vol. 141, No. 10 3842-3851
Copyright © 2000 by The Endocrine Society

ARTICLES

Estrogen Receptors {alpha} and ß in Rat Decidua Cells: Cell-Specific Expression and Differential Regulation by Steroid Hormones and Prolactin1

C. Tessier, S. Deb, A. Prigent-Tessier, S. Ferguson-Gottschall, G. B. Gibori, R. P. C. Shiu and G. Gibori

Department of Physiology and Biophysics, University of Illinois College of Medicine (C.T., S.D., A.P.-T., S.F.-G., G.B.G., G.G.), Chicago, Illinois 60612; and Department of Physiology, Faculty of Medicine, University of Manitoba (R.P.C.S.), Winnipeg, Manitoba, Canada R3E 0W3

Address all correspondence and requests for reprints to: Dr. Geula Gibori, Department of Physiology and Biophysics (M/C 901), University of Illinois, 835 South Wolcott Avenue, Chicago, Illinois 60612-7342. E-mail: ggibori{at}uic.edu

Estradiol is known to play an important role in the growth and differentiation of rat uterine stromal cells into decidual cells. In particular, this hormone with progesterone is necessary for blastocyst implantation and subsequent decidualization in the rat. Although binding experiments have demonstrated the presence of estrogen-binding sites, no evidence exists as to whether the rat decidua expresses both isoforms of the estrogen receptor (ER), {alpha} and ß. In this investigation, we analyzed the expression of decidual ER{alpha} and ERß, studied their regulation by PRL and steroid hormones and examined the ability of decidual ERß to transduce the estradiol signal to the progesterone receptor. Immunocytochemistry, RT-PCR, and Northern blot analysis showed that both ER species are coexpressed in the decidua during pseudopregnancy. Interestingly, these genes were preferentially found in a cell population localized in the antimesometrial site of the uterus where blastocyst implantation takes place. Using decidual cells in primary culture obtained from pseudopregnant rats and a decidua-derived cell line (GG-AD), we show a differential regulation of ER{alpha} and ERß by PRL and ovarian steroid hormones. Whereas PRL, estradiol, and progesterone all increased ERß messenger RNA (mRNA) expression in a dose-dependent manner, only PRL up-regulated the mRNA levels of ER{alpha}. Estradiol had no effect on ER{alpha} expression, whereas progesterone markedly decreased its mRNA levels. Interestingly, progesterone, which up-regulates the ability of PRL to signal to a PRL-regulated gene in mammary-gland derived cells, prevented PRL stimulation of decidual ER{alpha} and had no synergistic effect on ERß expression. The use of GG-AD cells, which express only ERß, allowed us to demonstrate that this receptor subtype is functional and transduces estradiol signal to the progesterone receptor. In summary, the results of this investigation have revealed that ERß is expressed in addition to ER{alpha} in the rat decidua, and that the expression of both ERs are cell specific and differentially regulated by PRL and steroids. One salient finding of this investigation is that progesterone down-regulates ER{alpha}, but concomitantly increases the expression of a functional ERß that mediates estradiol up-regulation of the decidual progesterone receptor.




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