Tsushima T, Arai M, Saji M, Ohba Y, Murakami H, Ohmura E, Sato K, Shizume K
Department of Medicine 2, Tokyo Women's Medical College, Japan.
Endocrinology. 1988 Aug;123(2):1187-94. doi: 10.1210/endo-123-2-1187.
The effect of transforming growth factor (TGF)-beta on DNA synthesis and iodine metabolism was studied in cultured porcine thyroid cells. TGF-beta 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-beta inhibits postreceptor events responsible for initiation of DNA synthesis. TGF-beta was a potent inhibitor of iodine metabolism. When porcine thyroid cells were cultured with TSH for 3 days in the presence of TGF-beta, TSH-induced iodide uptake and organification were reduced at rates that were dependent on the TGF-beta concentrations. The inhibition was detectable at TGF-beta concentrations as low as 50 pg/ml, and complete suppression was seen at 1 ng/ml. Only 6 h of exposure to TGF-beta resulted in a significant inhibition of TSH-induced iodine metabolism. Treatment of thyroid cells with TGF-beta for 3 days did not reduce cAMP production stimulated by TSH. Moreover, the intracellular cAMP level of thyroid cells cultured with TSH plus TGF-beta did not differ from that of cells cultured with TSH alone. TGF-beta decreased iodide uptake stimulated by forskolin or 8-bromo-cAMP. These results strongly suggest that TGF-beta inhibits TSH-stimulated iodine metabolism, at least in part, by affecting events subsequent to cAMP production. The physiological role of TGF-beta remains to be determined, but it may be involved in the regulation of thyroid cell growth and function.
在培养的猪甲状腺细胞中研究了转化生长因子（TGF）-β对DNA合成和碘代谢的影响。TGF-β剂量依赖性地抑制胰岛素样生长因子I和表皮生长因子刺激的DNA合成，但不影响这两种生长因子受体的数量或亲和力，这表明TGF-β抑制负责启动DNA合成的受体后事件。TGF-β是碘代谢的有效抑制剂。当猪甲状腺细胞在TGF-β存在下与促甲状腺激素（TSH）一起培养3天时，TSH诱导的碘摄取和有机化以依赖于TGF-β浓度的速率降低。在低至50 pg/ml的TGF-β浓度下即可检测到抑制作用，在1 ng/ml时可见完全抑制。仅暴露于TGF-β6小时就导致TSH诱导的碘代谢受到显著抑制。用TGF-β处理甲状腺细胞3天不会降低TSH刺激的环磷酸腺苷（cAMP）产生。此外，用TSH加TGF-β培养的甲状腺细胞的细胞内cAMP水平与仅用TSH培养的细胞的细胞内cAMP水平没有差异。TGF-β降低了福斯可林或8-溴-cAMP刺激的碘摄取。这些结果强烈表明，TGF-β至少部分地通过影响cAMP产生后的事件来抑制TSH刺激的碘代谢。TGF-β的生理作用尚待确定，但它可能参与甲状腺细胞生长和功能的调节。
