Oxidative stress induces the expression of Fas and Fas ligand and apoptosis in murine intestinal epithelial cells

被引:124
作者
Denning, TL
Takaishi, H
Crowe, SE
Boldogh, I
Jevnikar, A
Ernst, PB
机构
[1] Univ Virginia, Dept Internal Med, Charlottesville, VA 22908 USA
[2] Univ Texas, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77550 USA
[3] Univ Texas, Med Branch, Dept Pediat, Galveston, TX 77550 USA
[4] Univ Virginia, Digest Hlth Ctr Excellence, Charlottesville, VA USA
[5] Univ Western Ontario, Dept Microbiol & Immunol, London, ON, Canada
[6] Univ Western Ontario, Dept Med, London, ON, Canada
关键词
mucosal; inflammation; apoptosis; free radicals;
D O I
10.1016/S0891-5849(02)01141-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Intestinal epithelial cell function is compromised by local immune and inflammatory responses. In this study, we examined the possibility that intestinal epithelial cell injury occurs in the presence of activated inflammatory cells, such as neutrophils and macrophages, via production of reactive oxygen species (ROS). Following exposure to 50-150 muM H2O2, levels of mRNA and protein for Fas and, to a lesser degree, Fas-L were increased and intestinal epithelial cells underwent apoptosis. Treatment of H2O2-exposed cells with agonistic anti-Fas antibody, but not isotype control antibody, significantly enhanced apoptosis. Apoptosis was associated with the activation of caspase 8, while Z-IETD, an inhibitor of caspase 8, blocked apoptosis of H2O2-exposed intestinal epithelial cells. Thus, ROS induced Fas and Fas-L expression in association with intestinal epithelial cell apoptosis. These data support the hypothesis that, following exposure to oxidative stress, enterocytes are primed for cell death via Fas-mediated pathways. (C) 2002 Elsevier Science Inc.
引用
收藏
页码:1641 / 1650
页数:10
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