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Protein and Estrogen Responsiveness1
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
, ERß, and the
pituitary-specific ER 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 mRNA levels were not regulated significantly by any
treatment in vivo or in cell lines. However, E
suppressed ER protein levels in vivo and in cell
lines, and reduction of ER 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 protein and increases levels
of TERP-1 (which can suppress ER/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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