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Modulation of tissue plasminogen activator biosynthesis by phosphatidylinositol liposomes in human fetal lung fibroblasts
Author(s) -
Floru S.,
Gelvan A.,
Maran R.,
Kadouri A.,
Cohen A. M.
Publication year - 1991
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830360207
Subject(s) - biosynthesis , phosphatidylinositol , phosphatidylserine , phosphatidylethanolamine , activator (genetics) , phosphatidylcholine , phosphatidylglycerol , phospholipid , liposome , biochemistry , biology , microbiology and biotechnology , chemistry , signal transduction , receptor , enzyme , membrane
Phosphatidylinositol (PI) liposomes at 40 μM increased tissue plasminogen activator (t‐PA) biosynthesis by human fetal lung fibroblasts IMR‐90 (FLF), after 5 days of incubation by 7.4 ± 1.4 times of the control level. Other phospholipid liposomes, such as phosphatidylserine (PS), phosphatidylcholine (PC), and phosphatidylglycerol (PG), had no effect on t‐PA biosynthesis by FLF. The induction of t‐PA biosynthesis by PI liposomes was inhibited by specific inhibitors of phosphoinositide pathway: gentamycin and lithium chloride. Thus, gentamycin inhibited the effect of PI liposomes on t‐PA biosynthesis by 76% (P < 0.001), while it had no effect on control FLF. Likewise, lithium chloride inhibited t‐PA biosynthesis of both PI‐treated and control FLF by >84%. The induction of t‐PA biosynthesis by PI liposomes was dependent on RNA transcription and independent of DNA biosynthesis.