Analysis of mechanism for enhanced iodine uptake in thyrocytes by interferons

干扰素增强甲状腺细胞摄碘的机制分析

• 批准号: 08671023
• 负责人: MISAKI Takashi
• 金额: $ 1.41万
• 依托单位: KYOTO UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08671023/
• 关键词: interferons; thyrocytes; staurosporine; protein kinase C; iodine; C型り酸化酵素

In rat thyroid cell line FRTL5, thyroid stimulating hormone (TSH) stimulated protein kinase C (PKC) measured by binding of phorbol-dibutylate. Interferon (IFN) gamma dose dependently suppressed this stimulation. The suppression was reproduced by non-gamma IFN, and potentiated by tumor necrosis factor. On the other hand, inhibitors of PKC such as staurosporine, H-7, and H-9 stimulated iodine uptake in TSH-deprived FRTL5 cells, additive to IFN-driven enhancement. The 3 PKC inhibitors suppressed TSH stimulation of iodine uptake, while IFN act synergistically with TSH in this regard. The results imply IFN inhibits PKC activity via mechanisms different from that of other inhibitors.

在大鼠甲状腺细胞系FRTL 5中，促甲状腺激素（TSH）刺激蛋白激酶C（PKC）通过结合佛波酯来测量。干扰素（IFN）γ剂量依赖性抑制这种刺激。非γ干扰素复制的抑制，并增强肿瘤坏死因子。另一方面，PKC抑制剂如星形孢菌素、H-7和H-9刺激TSH剥夺的FRTL 5细胞中的碘摄取，添加到IFN驱动的增强。3种PKC抑制剂抑制TSH刺激碘摄取，而IFN在这方面与TSH协同作用。结果提示IFN抑制PKC活性的机制与其他抑制剂不同。

项目成果

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Misaki, T. et al.: "Unasual extrathyroidal uptake." Journal of Nuclear Medicine. 39; 9. 5A-1650 (1998)

Misaki, T. 等人：“异常的甲状腺外摄取。”