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1,25-Dihydroxyvitamin D₃ (1,25-(OH)₂D₃) is active in primary dispersed and clonal pituitary cells where it stimulates pituitary hormone production and agonist-induced hormone release. We have studied the effect of 1,25-(OH)₂D₃ on thyrotropin-releasing hormone (TRH) binding in clonal rat pituitary tumour (GH₃) cells. Compared with vehicle-treated cells, 1,25-(OH)₂D₃ (10 nmol/l) increased specific [³H]MeTRH binding by 26% at 8 h, 38% at 16 h, 35% at 24 h and reached a maximum at 48 h (90%). In dose–response experiments, specific [³H]MeTRH binding increased with 1,25-(OH)₂D₃ concentration and reached a maximum at 10 nmol/l. Half-maximal binding occurred at 0·5 nmol 1,25-(OH)₂D₃/l. The vitamin D metabolite, 25-OH D₃, increased [³H]MeTRH binding but was 1000-fold less potent than 1,25-(OH)₂D₃. In equilibrium binding assays, treatment with 10 nmol 1,25-(OH)₂D₃/l for 48 h increased the maximum binding from 67·4 ± 8·8 fmol/mg protein in vehicle-treated cells to 96·7 ± 12·4 fmol/mg protein in treated cells. There was no difference in apparent K_d (1·08 ± 0·10 nmol/l for 1,25-(OH)₂D₃-treated and 0·97 ± 0·11 nmol/l for vehicle-treated cells). Molecular investigations revealed that 10 nmol 1,25-(OH)₂D₃/l for 24 h caused an 8-fold increase in TRH receptor-specific mRNA. Actinomycin D (2 µg/ml, 6 h) abrogated the 1,25-(OH)₂D₃-induced increase in [³H]MeTRH binding. Cortisol also increased [³H]MeTRH binding but showed no additivity or synergism with 1,25-(OH)₂D₃. TRH-stimulated prolactin release was not enhanced by 1,25-(OH)₂D₃. We conclude that the active vitamin D metabolite, 1,25-(OH)₂D₃, caused a time- and dose-dependent increase in [³H]MeTRH binding. The effect was vitamin D metabolite-specific and resulted from an upregulation of the TRH receptor. Further studies are needed to determine the functional significance of this novel finding.

Journal of Endocrinology (1995) 147, 397–404

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