Peroxiredoxin III-deficiency Sensitizes Macrophages to Oxidative Stress

被引：31
作者：
Li, Lianqin [1 ,2 ]
Kaifu, Tomonori [3 ]
Obinata, Masuo [2 ]
Takai, Toshiyuki [3 ]
机构：
[1] Tsinghua Univ Second Hosp, Obstet & Gynecol Ctr, Beijing 100049, Peoples R China
[2] Tohoku Univ, Inst Dev Aging & Canc, Dept Cell Biol, Sendai, Miyagi 9808575, Japan
[3] Tohoku Univ, Inst Dev Aging & Canc, Dept Expt Immunol, Sendai, Miyagi 9808575, Japan
来源：
JOURNAL OF BIOCHEMISTRY | 2009年 / 145卷 / 04期
关键词：
lipopolysaccharide; macrophage; mouse; peroxiredoxin III; reactive oxygen species; NF-KAPPA-B; TNF-ALPHA; ANTIOXIDANT PROTEIN; LIPOPOLYSACCHARIDE; ACTIVATION; MITOCHONDRIA; THIOREDOXIN; REDUCTASE; CELLS; MICE;
D O I：
10.1093/jb/mvp011
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：
As a mitochondrial scavenger of reactive oxygen species (ROS), peroxiredoxin III (PrxIII) plays an important role in regulating intracellular ROS level. We previously found that PrxIII knockout (PrxIII(-/-)) mice were more sensitive than wild-type (PrxIII(+/+)) controls to intratracheal inoculation of lipopolysaccharide (LPS), but the precise mechanism remained to be obscure. In the present study, we detected the levels of ROS and tumour necrosis factor alpha (TNF-alpha) in mouse bone-marrow-derived macrophages. LPS stimulation induced transient increase of ROS production and augmentation of TNF-alpha accumulation in PrxIII(-/-) macrophages. In addition, we observed reduced viability and increased apoptosis in PrxIII(-/-) macrophages exposed to LPS. Our results provide direct evidence that PrxIII is necessary for macrophages to protect against LPS-induced oxidative stress.
引用
收藏
页码：425 / 427
页数：3
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