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Genome wide analysis of TNF-inducible genes reveals that antioxidant enzymes are induced by TNF and responsible for elimination of ROS

被引：28
作者：
Sasazuki, T
Okazaki, T
Tada, K
Sakon-Komazawa, S
Katano, M
Tanaka, M
Yagita, H
Okumura, K
Tominaga, N
Hayashizaki, Y
Okazaki, Y
Nakano, H
机构：
[1] Juntendo Univ, Sch Med, Dept Immunol, Bunkyo Ku, Tokyo 1138421, Japan
[2] Kyushu Univ, Grad Sch Med Sci, Dept Canc Therapy & Res, Higashi Ku, Fukuoka 8128582, Japan
[3] Kyushu Univ, Grad Sch Med Sci, Dept Surg & Oncol, Higashi Ku, Fukuoka 8128582, Japan
[4] JST, PRESTO, Kawaguchi, Saitama, Japan
[5] RIKEN, Yokohama Inst, Genom Sci Ctr, Lab Genome Explorat Res Grp,Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
来源：
MOLECULAR IMMUNOLOGY | 2004年 / 41卷 / 05期
基金：
日本学术振兴会;
关键词：
microarray; NF-kappa B; ROS; TNF; TRAF;
D O I：
10.1016/j.molimm.2004.03.030
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：
We recently showed that TNF induces accumulation of reactive oxygen species (ROS) that mediates necrosis in murine embryonic fibroblasts (MEFs) derived from TRAF2- and TRAF5-double deficient (DKO) mice. To elucidate the defects that subsequently cause accumulation of ROS in DKO MEFs, we compared gene expression profiles of wild-type and DKO MEFs before and after TNF stimulation using cDNA microarrays. Interestingly, many antioxidant enzymes are induced by TNF in wild-type MEFs, induction of these genes is impaired in DKO MEFs. Taken that TNF induces accumulation of ROS in DKO, but not wild-type MEFs, upregulation of antioxidant enzyme(s) might play a crucial role in elimination of ROS. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码：547 / 551
页数：5
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