Interleukin-1 inhibits thyrotrophin-induced human thyroglobulin gene expression

J Endocrinol. 1989 Jul;122(1):177-83. doi: 10.1677/joe.0.1220177.

Abstract

The regulation of thyroglobulin (Tg) and its specific mRNA by interleukin-1 (IL-1) in cultured human thyrocytes was investigated. Specific binding of 125I-labelled IL-1 on thyrocytes was confirmed by solid-phase binding assay. Thyrocytes dispersed from Graves' thyroid tissues were incubated with TSH with or without recombinant human IL-1. TSH stimulated Tg release from cultured human thyrocytes in a dose- and time-dependent manner. Both IL-1 alpha and beta inhibited TSH-induced Tg release at concentrations ranging from 0.01 to 10 U/ml. The suppressive activities of IL-1 alpha and beta were similar. They did not alter the basal level of Tg release. Unstimulated human thyrocytes did not contain any detectable Tg mRNA, but TSH-stimulated thyrocytes expressed a single species of Tg mRNA (8.5 kb). Both IL-1 alpha and beta inhibited TSH-induced Tg mRNA in a dose-responsive manner. IL-1 (10 U/ml) caused maximal suppression of TSH-induced Tg mRNA to nearly basal levels. In contrast, the gamma-actin mRNA hybridization signal was not altered in control or treated cells. Furthermore, IL-1 stimulated [3H]thymidine uptake into thyrocyte DNA. These results demonstrate that IL-1 directly inhibits TSH-induced Tg gene expression and provide further support for a functional role of IL-1 as a local modulator of thyroid hormone synthesis.

MeSH terms

  • Cells, Cultured
  • DNA / biosynthesis
  • DNA / drug effects
  • Gene Expression Regulation / drug effects*
  • Humans
  • Interleukin-1 / pharmacology*
  • RNA, Messenger / drug effects
  • Recombinant Proteins / pharmacology
  • Thyroglobulin / genetics*
  • Thyroid Gland / drug effects
  • Thyroid Gland / metabolism
  • Thyrotropin / antagonists & inhibitors*

Substances

  • Interleukin-1
  • RNA, Messenger
  • Recombinant Proteins
  • Thyrotropin
  • DNA
  • Thyroglobulin