Nuclear translocation of estrogen-receptor complex and stimulation of RNA synthesis by estrogens of different biological potencies in the female rat pituitary.
Stimulation of RNA synthesis and of nuclear translocation of estrogen-receptor complexes was investigated in isolated nuclei of anterior pituitaries of castrated female rats after injection with estrogens of different biological potencies. The assay system for the estimation of total RNA synthesis was validated and data suggest that incorporation of [3H]UMP into acid-precipitable material is consistent with RNA synthesis. An increase in RNA synthesis was seen 30 min after application of either 17 beta-estradiol, estriol or 1,3-diacetyl-17 alpha-ethinyl-7 alpha-methyl-1,3,5,(10)estratriene-17,3-ol (DMEE). RNA synthesis was maximal 90 min after estrogen application. Thereafter, RNA synthesis decreased slowly and reached pretreatment levels 3, 8 and 30 h after application of estriol, 17 beta-estradiol and the diacetyl derivative of ethinyl-estradiol, respectively. All estrogens were found to stimulate rapidly nuclear translocation of estrogen-receptor complexes. Peak levels of nuclear receptor contents were reached 30 min after administration of estrogens. A concomitant depletion of cytosol receptor levels was noted. Nuclear retention of estrogen-receptor complexes paralelled duration of enhanced RNA synthesis and correlated with biological potencies of the steroids. Data of present experiments combine to suggest that long-term nuclear retention is a requisite for expression of biological activity of estrogens at the anterior pituitary. Furthermore, the degree of biological activity seems to be associated with duration of stimulation of RNA synthesis, amount of estrogen-receptor complexes translocated to the nucleus, and duration of nuclear retention.
D000818:Animals; D001692:Biological Transport; D002467:Cell Nucleus / Q000378:metabolism*; D002940:Circadian Rhythm; D003600:Cytosol / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D045166:Estradiol Congeners / Q000494:pharmacology*; D004964:Estriol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D004997:Ethinyl Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D012313:RNA / Q000096:biosynthesis*; D051381:Rats; D011960:Receptors, Estrogen / Q000378:metabolism*
D045166:Estradiol Congeners; D004967:Estrogens; D011960:Receptors, Estrogen; D004997:Ethinyl Estradiol; D004958:Estradiol; D012313:RNA; C025040:1,3-diacetyl-17 alpha-ethinyl-7 alpha-methyl-1,3,5(10)estratriene-17,3-ol; D004964:Estriol