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Estrogen Receptor Signaling Pathways Differentially Regulate Gonadotropin Subunit Gene Expression and Serum Follicle-Stimulating Hormone in the Female Mouse

Department of Medicine (C.G.-K., J.W., L.A.H., J.L.J.), Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; and Department of Neurobiology and Physiology (J.E.L.), Weinberg College of Arts and Sciences, Northwestern University, Evanston, Illinois 60208

Address all correspondence and requests for reprints to: Dr. J. Larry Jameson, Morton Building 4-656, 303 East Chicago Avenue, Chicago, Illinois 60611-3008. E-mail: ljameson{at}northwestern.edu.

Estrogen, acting via estrogen receptor (ER), regulates serum gonadotropin levels and pituitary gonadotropin subunit expression. However, the cellular pathways mediating this regulation are unknown. ER signals through classical estrogen response element (ERE)-dependent genomic as well as nonclassical ERE-independent genomic and nongenomic pathways. Using targeted mutagenesis in mice to disrupt ER DNA binding activity, we previously demonstrated that ERE-independent signaling is sufficient to suppress serum LH levels. In this study, we examined the relative roles of ERE-dependent and -independent estrogen signaling in estrogen regulation of LH, FSH, prolactin, and activin/inhibin subunit gene expression, pituitary LH and FSH protein content, and serum FSH levels. ERE-independent signaling was not sufficient for estrogen to induce pituitary prolactin mRNA or suppress pituitary LHβ mRNA, LH content, or serum FSH in estrogen-treated ovariectomized mice. However, ERE-independent signaling was sufficient to reduce pituitary glycoprotein hormone -subunit, FSHβ, and activin-βB mRNA expression. Together with previous serum LH results, these findings suggest ERE-independent ER signaling suppresses serum LH via reduced secretion, not synthesis. Additionally, ERE-dependent and ERE-independent ER pathways may distinctly regulate steps involved in the synthesis and secretion of FSH.

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