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- Title
Lipopolysaccharide and interferon-γ enhance Fas-mediated cell death in mouse vascular endothelial cells via augmentation of Fas expression.
- Authors
Koide, N.; Morikawa, A.; Tumurkhuu, G.; Dagvadorj, J.; Hassan, F.; Islam, S.; Naiki, Y.; Mori, I.; Yoshida, T.; Yokochi, T.
- Abstract
The effect of interferon (IFN)-γ and/or lipopolysaccharide (LPS) on Fas-mediated cell death with anti-Fas agonistic antibody in vascular endothelial cells was examined using a mouse END-D cell line. Anti-Fas agonistic antibody exhibited cytotoxic actions on END-D cells. Fas-mediated cell death was enhanced by LPS or IFN-γ. The combination of IFN-γ and LPS significantly enhanced cell death compared to IFN-γ or LPS alone. IFN-γ and LPS augmented cell surface expression of Fas, but not tumour necrosis factor (TNF) receptor 1. Inhibitors of p38 mitogen-activated protein kinase (MAPK) prevented augmentation of Fas expression in IFN-γ and LPS-treated END-D cells. IFN-γ and LPS-treated END-D cells did not become susceptible to TNF-α or nitric oxide-mediated cytotoxicity. IFN-γ and LPS thus appear to augment selectively Fas expression via activation of p38 MAPK and enhance Fas-mediated cell death in END-D cells. Furthermore, administration of IFN-γ and LPS into mice induced in vivo expression of Fas on vascular endothelial cells and Fas ligand (FasL) on peripheral blood leucocytes. The relationship between enhancement of Fas-mediated cell death by IFN-γ and LPS and the development of vascular endothelial injury is discussed.
- Subjects
INTERFERONS; ENDOTOXINS; CELL death; GENE expression; CELL-mediated cytotoxicity
- Publication
Clinical & Experimental Immunology, 2007, Vol 150, Issue 3, p553
- ISSN
0009-9104
- Publication type
Article
- DOI
10.1111/j.1365-2249.2007.03499.x