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Université de Rennes I, Interactions Cellulaires et Moléculaires, Centre National de la Recherche Scientifique, UMR 6026, Campus de Beaulieu, 35042 Rennes, France
Address all correspondence and requests for reprints to: Dr. M.-L. Thieulant, Equipe d’Information et Programmation Cellulaire, UMR 6026, Batiment 13, Campus de Beaulieu, 35042 Rennes Cedex, France. E-mail: marie-lise.thieulant{at}univ-rennes1.fr
In the rat pituitary gland the mechanism responsible for ER
regulation has not been fully elucidated. Using transient transfection
assays in T3–1 cells, a cell line of gonadotrope origin, we show
that GnRH stimulates estrogen response element-containing promoters in
an estrogen-independent manner. This effect was strictly ER and GnRH
receptor dependent, as no activation of the reporter gene was observed
in presence of the anti-estrogen ICI 182,780 or a GnRH antagonist.
These data suggest that the GnRH-triggered signaling pathway results in
17ß-estradiol-independent trans-activation of the
ER in T3–1 cells. Furthermore, an additive activation was
achieved when cells were treated with both GnRH and 17ß-estradiol. In
primary pituitary cells, GnRH alone (100 nM) did not cause
a significant stimulation of reporter gene activity, presumingly due to
the low amount of gonadotropes. Interestingly, the combination of
17ß-estradiol and GnRH resulted in a significant increase in ER
trans-activation compared with that in cells treated
with 17ß-estradiol alone. This enhancement was prevented by ICI
182,780, showing an ER requirement. Moreover, we show that the
effects of GnRH on ER transcriptional activity in gonadotrope cell
lines are mediated by the PKC/MAPK pathway. In conclusion, our data
demonstrate that GnRH is an important signal in the regulation of ER
trans-activation in gonadotrope cells.
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