17 beta-Estradiol regulates prolactin secretion but not cell proliferation of GH3B6 cells in chemically defined...

The effects of 17 beta-estradiol on proliferation and prolactin secretion by a clonal rat pituitary cell, GH3B6, have been investigated in a chemically defined medium (Ham's F12, transferrin, insulin and parathyroid hormone). Under these conditions, 17 beta-estradiol alone (5 X 10(-14)-5 X 10(-9) M) was not a mitogen for GH3B6 cells as shown by cell counts and DNA measurements. However, it slowed down the drop in prolactin production induced by culture in this chemically defined medium. After 3 and 7 days it stimulated PRL production up to 5 times in a dose-dependent manner. This secretory response was abolished by tamoxifen, and not mimicked by progesterone, testosterone or dexamethasone. The thyroliberin-induced stimulation of prolactin production occurred more rapidly (24 h) than and was additive to the 17 beta-estradiol response, suggesting that these two factors act through independent mechanisms. PRL neosynthesis in culture was attested to by the incorporation of [35S]methionine (5 h) into immunoprecipitable prolactin. Neither 17 beta-estradiol nor thyroliberin increases specifically prolactin radioactivity, although they strongly decreased the specific activity of prolactin in both cells and medium. This suggests that they mostly acted by decreasing PRL turnover rate.