Effects of estrogen and progesterone on cytoplasmic estrogen receptor and rates of protein synthesis in rat uterus

P. B. CouLson, E. J. Pavlik

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38 Scopus citations


Changes in total cytoplasmic estrogen receptor (E2-Rc) concentrations were compared to changes in rates of protein synthesis after steroid treatment in uterine tissue of long-term castrate Sprague Dawley rats. Animals were treated with estradiol 17β (E2) alone or with progesterone (P4) after 24 h of E2 "priming". E2-Rc concentration was "modulated" by E2 (0.1 μg I.P.) in two distinct temporal phases: (A) Short term depletion with restoration to basal E2-Rc/mg DNA occurred by 20 h after E2 treatment. (B) Increases in E2-Rc above basal levels were seen after 20-24 h. Twenty-four h after E2 treatment, the administration of P4 (1.0 mg s.c.) caused the elevated concentration of total E2-Rc to decrease to base line levels within 2h. As determined from E2-Rc decay experiments, modulation of E2-Rc by E2 or P4 was not caused by activation of some soluble cytoplasmic receptor precursor nor by degradation (through proteolytic enzymes) of functional E2-Rc. Uterine protein synthesis was monitored by pulse-labeling with [35S]-methionine under the same treatment schedule as used for E2-Rc quantitation. Both E2 and P4 stimulated incorporation of [35S]-methionine into ribosomal, cytoplasmic and nuclear fractions. Increases in rates of [35S]-methionine incorporation were interpreted as a demonstration of "hypertrophy". Since hypertrophy accompanied treatment with both estradiol and progesterone, and since differential modulation of E2-Rc followed treatment with these steroids, the increase in E2-Rc concentration following E2 treatment appears to be a specific event which is distinct from hypertrophy. It is proposed that estrogen mediated increases in E2Rc concentration represent a mechanism of molecular amplification which contributes in part to the cascading growth observed in the uterus. Conversely, progesterone antagonizes estrogen stimulation by depleting E2-Rc concentration (in some unknown manner) thereby providing a biochemical "brake" to estrogen stimulation.

Original languageEnglish
Pages (from-to)205-212
Number of pages8
JournalJournal of Steroid Biochemistry
Issue number3
StatePublished - Mar 1977

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology


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