Modulation of fibrinolytic activity produced by t98g glioblastoma cells by inflammatory mediators and dexamethasone

Etsuo Yoshida*, Sayuri Ohmura, Jiro Kawano, Masahiko Sugiki, Masugi Maruyama, Hau C. Kwaan

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

Plasminogen-plasmin system play important roles in regulating tumor invasion, tissue remodeling and neovascularization. We investigated the effect of various cytokines on fibrinolytic activity produced by T98G glioblastoma cells. Cytokines used were interleukin(IL)-la and b, IL-2, IL-3, IL-4, IL-6, tumor necrotic factor (TNF) a and b. Highest fibrinolytic activity measured by fibrin autography was observed in the conditioned medium of T98G cells treated by IL-la and TNFa. IL-4 and IL-6 produced a slight increase in fibrinolytic activity, while IL-2 and IL-3 had little effect. Dexamethasone decreased significantly the fibrinolytic activity. Zymographic analysis and ELISA showed that the increased fibrinolytic activity induced by IL-ls and TNFs were caused by increased urokinase-type plasminogen activator secretion, and that decreased activity induced by dexamethasone was caused by a decrease in urokinase-type plasminogen activator and an increase in type-1 plasminogen activator inhibitor secretion.

Original languageEnglish (US)
Number of pages1
JournalFibrinolysis
Volume10
Issue numberSUPPL. 3
DOIs
StatePublished - 1996

ASJC Scopus subject areas

  • Hematology

Fingerprint Dive into the research topics of 'Modulation of fibrinolytic activity produced by t98g glioblastoma cells by inflammatory mediators and dexamethasone'. Together they form a unique fingerprint.

  • Cite this