Thyrotropin releasing hormone receptors in regulation of prolactin gene expression in GH cells

Abstract Three GH cell strains (rat pituirary tumor cells in culture) which synthesize different amounts of prolactin (PRL) and which exhibit a differential response to thyrotropin releasing hormone (TRH), have been utilized to study the TRH receptor-modulated regulation of PRL gene expression. Equilibrium [ 3 H]TRH binding studies revealed that, PRL-producing (PRL + ) GH 4 C 1 and 928-9b GH substrains possess TRH specific receptors with similar affinities for the ligand. However the total number of TRH receptors per cells in TRH-nonresponsive 928-9b strain is 6.5 fold lower than that could be detected in TRH-responsive GH 4 C 1 cells. Epidermal growth factor (EGF) also stimulates PRL synthesis in GH 4 C 1 cells. Unlike TRH, EGF stimulates PRL synthesis in TRH-nonresponsive 928-9b cells, suggesting that nuclear events necessary for the stimulation of PRL gene expression in 928-9b cells are operative. 5 Bromodeoxyuridine (BrdUrd) induces PRL synthesis in PRL-nonproducing (PRL − ) F 1 BGH 1 2C 1 cells. PRL induction in BrdUrd-treated cells can not be further stimulated by TRH or EGF.