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Endocrinology Vol. 141, No. 6 2174-2184
Copyright © 2000 by The Endocrine Society

ARTICLES

Differential Expression and Regulation of Estrogen Receptors (ERs) in Rat Pituitary and Cell Lines: Estrogen Decreases ER{alpha} Protein and Estrogen Responsiveness1

Derek A. Schreihofer, Mark H. Stoler and Margaret A. Shupnik

Department of Internal Medicine, Division of Endocrinology and Metabolism, and Department of Pathology (M.H.S.), University of Virginia, Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Margaret A. Shupnik, Ph.D., Box 800578, Department of Internal Medicine, University of Virginia Health Science Center, Charlottesville, Virginia 22908. E-mail: mas3x{at}virginia.edu

Estrogen (E) regulates the synthesis and secretion of several pituitary hormones during the reproductive cycle in a cell- and promoter-specific manner. One mechanism underlying cell specificity is the differential expression of estrogen receptor (ER) isoforms. We used in vivo and in vitro rodent pituitary cell models to examine the expression and regulation of ER{alpha}, ERß, and the pituitary-specific ER{alpha} isoform, truncated estrogen receptor product-1 (TERP-1). In cycling female rat pituitaries, ERß messenger RNA (mRNA) levels fell 40% on the morning of proestrus and were suppressed by E or dihydrotestosterone in ovariectomized females. In lactotrope and gonadotrope cell lines (GH3, RC4B, LßT2), progesterone (P) or P plus E also suppressed ERß. TERP-1 mRNA increased 3-fold at proestrus and in response to E treatment in vivo and in cell lines. ER{alpha} mRNA levels were not regulated significantly by any treatment in vivo or in cell lines. However, E suppressed ER{alpha} protein levels in vivo and in cell lines, and reduction of ER{alpha} protein levels by E or the antiestrogen ICI182,780 reduced E-stimulated transcriptional activation of the PRL promoter in GH3 cells. TERP-1 and ERß protein levels were low to undetectable in cell lines, but E stimulated TERP-1. Because E treatment decreases ERß mRNA and ER{alpha} protein and increases levels of TERP-1 (which can suppress ER{alpha}/ß activity), the dynamic steroid-induced changes in ER expression in the rat pituitary during the midcycle gondaotropin/PRL surge may provide a means for ovarian steroids to limit positive feedback.




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