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

doi:10.1016/s0268-9499(96)80569-8

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

Medicine, Hematology Oncology Division

Research output: Contribution to journal › Article › peer-review

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 language	English (US)
Number of pages	1
Journal	Fibrinolysis
Volume	10
Issue number	SUPPL. 3
DOIs	https://doi.org/10.1016/s0268-9499(96)80569-8
State	Published - 1996

ASJC Scopus subject areas

Hematology

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10.1016/s0268-9499(96)80569-8

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@article{ba849fe8925d46c0a6aa0970ad17b1ac,

title = "Modulation of fibrinolytic activity produced by t98g glioblastoma cells by inflammatory mediators and dexamethasone",

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.",

author = "Etsuo Yoshida and Sayuri Ohmura and Jiro Kawano and Masahiko Sugiki and Masugi Maruyama and Kwaan, {Hau C.}",

year = "1996",

doi = "10.1016/s0268-9499(96)80569-8",

language = "English (US)",

volume = "10",

journal = "Fibrinolysis",

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T1 - Modulation of fibrinolytic activity produced by t98g glioblastoma cells by inflammatory mediators and dexamethasone

AU - Yoshida, Etsuo

AU - Ohmura, Sayuri

AU - Kawano, Jiro

AU - Sugiki, Masahiko

AU - Maruyama, Masugi

AU - Kwaan, Hau C.

PY - 1996

Y1 - 1996

N2 - 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.

AB - 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.

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U2 - 10.1016/s0268-9499(96)80569-8

DO - 10.1016/s0268-9499(96)80569-8

M3 - Article

AN - SCOPUS:33846695889

SN - 0268-9499

VL - 10

JO - Fibrinolysis

JF - Fibrinolysis

IS - SUPPL. 3

ER -

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

Abstract

ASJC Scopus subject areas

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