Estrogen Receptors α and β in Rat Decidua Cells: Cell-Specific Expression and Differential Regulation by Steroid Hormones and Prolactin1

• Published in: Endocrinology (Philadelphia) Vol. 141; no. 10; pp. 3842 - 3851
• Main Authors: Tessier, C, Deb, S, Prigent-Tessier, A, Ferguson-Gottschall, S, Gibori, G. B, Shiu, R. P. C, Gibori, G
• Format: Journal Article
• Language: English
• Published: Endocrine Society 01-10-2000
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/endo.141.10.7734

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), α and β. In this
investigation, we analyzed the expression of decidual ERα and ERβ,
studied their regulation by PRL and steroid hormones and examined the
ability of decidual ERβ 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
ERα and ERβ by PRL and ovarian steroid hormones. Whereas PRL,
estradiol, and progesterone all increased ERβ messenger RNA (mRNA)
expression in a dose-dependent manner, only PRL up-regulated the mRNA
levels of ERα. Estradiol had no effect on ERα 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 ERα and had no synergistic effect on ERβ
expression. The use of GG-AD cells, which express only ERβ, 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 ERβ is expressed
in addition to ERα 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 ERα, but concomitantly increases the
expression of a functional ERβ that mediates estradiol up-regulation
of the decidual progesterone receptor.