Estrogen Stimulates Prolactin Gene Transcription by a Mechanism Independent of Pituitary Protein Synthesis*

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Abstract
An in vitro nuclear transcription system was used to investigate the mechanisms through which 17.beta.-estradiol regulates PRL [prolactin] gene expression in the rat pituitary. A single injection of this estrogen stimulated the rate of PRL RNA synthesis in nuclei isolated from male rats within 30 min of treatment, and this stimulated rate of PRL RNA synthesis was observed for at least 48 h after injection. In contrast, estrogen treatment had little effect on the rate of GH [growth hormone] RNA synthesis. Cycloheximide, at a dose sufficient to inhibit pituitary protein synthesis by greater than 80%, did not block this estradiol-mediated stimulation of PRL RNA synthesis through at least the first 8 h after hormone treatment. Estradiol treatment also resulted in a rapid transformation of the pituitary estrogen receptors from the cytosolic to the nuclear form. However, the level of receptor in the nuclear form peaked within 1 h and had returned to near the control value within 6 h of hormone injection. Apparently 17.beta.-estradiol regulates PRL gene transcription through a mechanism independent of pituitary protein synthesis. In addition, the rates of PRL RNA synthesis over the time course examined were not correlated with the percentage of the pituitary estrogen receptor population existing in the nuclear form.