Thyrotropin-stimulated iodide transport mediated by adenosine 3',5'-monophosphate and dependent on protein synthesis.

Abstract

Iodide (I-) uptake by FRTL-5 cells, a functioning rat thyroid cell line, is TSH dependent. The effects of TSH withdrawal are not apparent until 1 day; 1 week is required to reduce I- uptake to a minimal level. The readdition of TSH leads to a return of the I--concentrating ability after a latency of 12-24 h. The reappearance of I- uptake induced by TSH is mimicked by (Bu)2cAMP and agents that elevate intracellular cAMP levels in these cells, such as forskolin, cholera toxin, and a Graves' disease serum. The appearance of I- uptake after TSH occurs 12 h after the appearance of TSH-induced [35S]methionine incorporation. Cycloheximide blocks both the TSH- and (Bu)2cAMP-induced increases in methionine incorporation and I- uptake to the same extent and in an identical concentration-dependent manner. TSH-induced [35S]methionine incorporation is associated with increased radiolabeling of several specific proteins, as revealed by gel electrophoresis; none, however, is radiolabeled coincident in time with the appearance of TSH-induced I- uptake. Several proteins whose apparent synthesis is induced by TSH also exhibit TSH-dependent phosphorylation.