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Plasminogen activator inhibitor type 1 biosynthesis and mRNA level are increased by dexamethasone in human fibrosarcoma cells.
Author(s) -
P.A. Andreasen,
Charles Pyke,
Andrea Riccio,
Peter Kristensen,
Lene Nielsen,
Leif R. Lund,
Francesco Blasi,
Keld Danø
Publication year - 1987
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.7.8.3021
Subject(s) - cycloheximide , plasminogen activator , biology , dexamethasone , biosynthesis , messenger rna , extracellular , plasminogen activator inhibitor 1 , cell culture , endocrinology , fibrosarcoma , microbiology and biotechnology , medicine , activator (genetics) , enzyme , protein biosynthesis , biochemistry , gene , genetics
Dexamethasone increases type 1 plasminogen activator inhibitor (PAI-1) activity released from the human fibrosarcoma cell line HT-1080. We demonstrated that dexamethasone caused about 10-fold increases in the intracellular and extracellular levels of PAI-1 protein, as measured by an enzyme-linked immunosorbent assay, in the rate of PAI-1 biosynthesis, and in the PAI-1 mRNA level. The effects on PAI-1 biosynthesis and mRNA level were detectable within 4 h and were maximal 16 to 24 h after the addition of dexamethasone. Cycloheximide did not inhibit the dexamethasone-induced increases in the capacity of the cells to synthesize PAI-1 and in the PAI-1 mRNA level.

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