Studies on the control of plasminogen activator production by cultured human embryonic lung cells: requirements for inhibition by corticosteroids.
The ability of actinomycin D to interfere with the dexamethasone-mediated inhibition of plasminogen activator (PA) production by human-embryonic lung (HuEL) cells has been examined. The enzyme produced by HuEL cells in the presence of both dexamethasone and actinomycin D appears to be the product of de novo protein synthesis, as determined by the dependence of PA production on active protein synthesis and the net increase in total PA during the course of an experiment. Inhibition of RNA synthesis must be continuous to maintain PA production in the presence of dexamethasone, since reinitiation of RNA synthesis causes an immediate loss of PA activity in the cells. Cordycepin and alpha-amanitin also prevent dexamethasone-mediated inhibition of PA in HuEL cells, indicating that the RNA whose synthesis must be prevented is of the mRNA class. These experiments imply that PA production in HuEL cells may be under translational as well as transcriptional control.
D002478:Cells, Cultured; D003609:Dactinomycin / Q000494:pharmacology; D003907:Dexamethasone / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D006801:Humans; D008168:Lung / Q000201:enzymology* / Q000378:metabolism; D010960:Plasminogen Activators / Q000096:biosynthesis*; D014176:Protein Biosynthesis / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects
D012333:RNA, Messenger; D003609:Dactinomycin; D003907:Dexamethasone; D010960:Plasminogen Activators