Rapoport B, Filetti S, Takai N A
Endocrinology. 1983 May;112(5):1874-6. doi: 10.1210/endo-112-5-1874.
In contrast to our previous experience with cultured thyroid cells, cycloheximide, actinomycin D and nicotinamide did not prevent TSH-induced desensitization in dog thyroid cells in primary culture for only one day. With continued duration of culture prevention of TSH desensitization by these agents did emerge, but asynchronously. Thus on the second day of primary culture, while cycloheximide and actinomycin D prevented TSH desensitization, nicotinamide remained ineffective. On the third day of primary culture all three agents blocked TSH desensitization. Examination of precursor incorporation into newly synthesized DNA, RNA and protein revealed a temporal association between the appearance of susceptibility to inhibition of TSH desensitization and an increase in DNA and protein synthesis. These data provide an explanation for the discrepant reports regarding the effect of protein synthesis inhibitors on TSH desensitization.
与我们之前在培养甲状腺细胞方面的经验相反,放线菌酮、放线菌素D和烟酰胺并不能阻止促甲状腺激素(TSH)诱导的原代培养仅一天的犬甲状腺细胞脱敏。随着培养时间的延长,这些试剂对TSH脱敏的预防作用确实出现了,但并不同步。因此,在原代培养的第二天,虽然放线菌酮和放线菌素D阻止了TSH脱敏,但烟酰胺仍然无效。在原代培养的第三天,所有三种试剂都阻断了TSH脱敏。对新合成的DNA、RNA和蛋白质中前体掺入的检查揭示了对TSH脱敏抑制敏感性的出现与DNA和蛋白质合成增加之间的时间关联。这些数据为关于蛋白质合成抑制剂对TSH脱敏作用的矛盾报道提供了解释。