In vitro studies have demonstrated a progesterone-induced activity associated with the uterine nuclear fraction which resulted in the loss of nuclear estrogen receptor. Uterine nuclear suspension or nuclear KC1 (0.5 M) extract from control and progesterone-treated (30 min or 2h) hamsters were incubated at 37 C for 0, 15, or 30 min in Tris-glycerol buffer. Preparations from progesterone-treated hamsters showed an accelerated reduction of total estrogen receptor which was primarily due to preferential loss of occupied receptor. This progesterone-dependent stimulation of estrogen receptor loss was absent when nuclear extract was prepared in phosphate buffer rather than Tris buffer. In addition, sodium molybdate and sodium metavanadate (both at 10 mM) inhibited this activity in nuclear extract. These observations support the hypothesis that progesterone modulation of estrogen action may be accomplished by induction (or activation) of an estrogen receptor-regulatory factor (Re-RF), and this factor may in turn act to eliminate the occupied form of estrogen receptor from the nucleus, perhaps through a hypothetical dephosphorylation-inactivation mechanism.
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