作者: L. R. Lund , A. Riccio , P. A. Andreasen , L. S. Nielsen , P. Kristensen
DOI: 10.1002/J.1460-2075.1987.TB02365.X
关键词:
摘要: We have studied the mechanism of a transforming growth factor-beta (TGF-beta)-stimulated production type-1 plasminogen activator inhibitor (PAI-1) in WI-38 human lung fibroblasts. TGF-beta causes an early increase PAI-1 mRNA level which reaches maximal 50-fold enhancement after 8 h. Blocking protein synthesis with cycloheximide equally strong mRNA. Quantitative studies effect on levels cell extracts and culture media by using monoclonal antibodies are consistent The results suggest primary gene transcription, also possibility that transcription this non-induced cells may be suppressed short-lived negatively regulating protein. Urokinase-type (u-PA) tissue-type (t-PA) activators decreased TGF-beta-treated concomitantly accumulation. These findings show important biological overall extracellular proteolytic activity, give insight into molecular mechanisms underlying action at genetic level.