Thyroid Hormone Specifically Inhibits Prolactin Synthesis and Decreases Prolactin Messenger Ribonucleic Acid Levels in Cultured Pituitary Cells*

Abstract

Electrophoretic analysis of soluble proteins from pituitary cells pulse labeled with [³⁵S]methionine demonstrated that 10 nM T₃ inhibited PRL synthesis, but did not affect the synthesis of most other pituitary proteins. The effects of T₃ were somewhat slow, requiring about 3 days for a 50% reduction in PRL synthesis. PRL synthesis slowly returned toward control levels after the removal of T₃ from the culture medium. In serum-free medium, a concentration of about 0.6 nM T₃ was required for half-maximal inhibition of PRL synthesis. In medium containing 5% fetal calf serum, only slightly higher concentrations of T₃ were required to inhibit PRL synthesis. The K_d for the binding of [¹²⁵I]T₃ to pituitary cell nuclei was 0.2 nM. Analysis of PRL mRNA levels by hybridization of total cellular RNA to PRL cDNA demonstrated that there was a good correspondence between T₃ effects on PRL synthesis and PRL mRNA. These findings demonstrate that T₃ can specifically inhibit PRL synthesis and PRL mRNA levels in cultured pituitary cells and suggest that T₃ may have a physiological role in the regulation of PRL synthesis.