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Department of Medicine 2, Tokyo Women's Medical College and Institute for Growth Science Megumi Miyakawa, 8–1, Kawada-cho, Shinjuku-ku, Tokyo 162, Japan
Address correspondence and requests for reprints to: Dr. Toshio Tsushima, Department of Medicine 2, Tokyo Women's Medical College, 8–1, Kawada-cho, Shinjuku-ku, Tokyo 162, Japan.
Abstract
The effect of transforming growth factor (TGF)-β on DNA synthesis and iodine metabolism was studied in cultured porcine thyroid cells. TGF-β dose-dependently inhibited DNA synthesis stimulated by both insulin-like growth factor I and epidermal growth factor but did not affect the number or affinity of receptors for the two growth factors, suggesting that TGF-β inhibits postreceptor events responsible for initiation of DNA synthesis. TGF-β was a potent inhibitor of iodine metabolism. When porcine thyroid cells were cultured with TSH for 3 days in the presence of TGF-β, TSH-induced iodide uptake and organification were reduced at rates that were dependent on the TGF-0 concentrations. The inhibition was detectable at TGF-β concentrations as low as 50 pg/ml, and complete suppression was seen at 1 ng/ml. Only 6 h of exposure to TGF-β resulted in a significant inhibition of TSH-induced iodine metabolism. Treatment of thyroid cells with TGF-β for 3 days did not reduce cAMP production stimulated by TSH. Moreover, the intracellular cAMP level of thyroid cells cultured with TSH plus TGFβdid not differ from that of cells cultured with TSH alone. TGF-β decreased iodide uptake stimulated by forskolin or 8-bromo-cAMP. These results strongly suggest that TGF-β inhibits TSH-stimulated iodine metabolism, at least in part, by affecting events subsequent to cAMP production. The physiological role of TGF-β remains to be determined, but it may be involved in the regulation of thyroid cell growth and function. (Endocrinology 123: 1187–1194, 1988)
Footnotes
* This work was supported by grants from the Ministry of Education and the Ministry of Health and Welfare.
Received January 19, 1988.
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