Article révisé par les pairs
Résumé : The possibility that TSH is required for maintenance of thyroglobulin (TG) messenger RNA (mRNA) levels in the thyroid was tested by producing TSH deficiency in Wistar Furth rats. Concentrations of TG mRNA in the thyroid cytoplasmic RNAs of treated and control rats were compared by the relative rates of hybrid formation with TG complementary DNA. The products of the concentration of the TG mRNA times the amount of RNA per thyroid DNA were used to compare the amounts of TG mRNA on a cellular basis in each test condition. The results showed that rats made TSH-deficient either by suppression with high doses of T4 (100–150 μg daily–100 g BW for 7–10 days) or by hypophysectomy underwent a decrease in amount of TG mRNA in excess of the diminution of other RNA classes. The RNA content of the cytoplasm decreased by 32–38% in four groups of T4-treated animals, whereas the cytoplasmic TG mRNA content decreased by 62–70%. In four groups of hypophysectomized animals, fractional changes were more variable, with the cytoplasmic RNA declining by 31–51% in 5–6 days, whereas the TG mRNA content decreased by 65–92%. Although TSH deficiency consistently decreased the concentration of TG mRNA, the proportion of total messenger RNA, measured as the RNA poly (A) content, was increased by more than 25%. A relative conservation of the majority of other thyroid messengers in the T4-suppressed state was also indicated by the translational efficiency of the RNAs and shown qualitatively by the distribution of the translational products in two-dimensional electrophoresis. Administration of TSH to the hypophysectomized rats maximally increased the cellular RNA 2.4 times above the baseline, hypophysectomized condition. Coincidental increases in the cellular TG mRNA content ranged between 6.7- and 14-fold. The results show that in TSH deficiency, decreases of TG mRNA occur to a greater extent than that of other thyroid messengers. Moreover, one consequence of TSH-stimulation of thyroid depleted of the TG mRNA is the reaccumulation of that messenger. © 1981 by The Endocrine Society.