Differential effect of protein synthesis inhibition on TSH desensitization at different stages of primary thyroid cell culture.
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.
D000818:Animals; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D003513:Cycloheximide / Q000494:pharmacology*; D004261:DNA Replication / Q000187:drug effects; D003609:Dactinomycin / Q000494:pharmacology*; D004285:Dogs; D007700:Kinetics; D009536:Niacinamide / Q000494:pharmacology; D014176:Protein Biosynthesis / Q000187:drug effects*; D013961:Thyroid Gland / Q000187:drug effects / Q000502:physiology*; D013972:Thyrotropin / Q000494:pharmacology*; D014158:Transcription, Genetic / Q000187:drug effects
D003609:Dactinomycin; D009536:Niacinamide; D013972:Thyrotropin; D003513:Cycloheximide; D000242:Cyclic AMP