Journal of Biochemistry Advance Access published online on January 20, 2009
Journal of Biochemistry, doi:10.1093/jb/mvp011
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Rapid Communication |
Peroxiredoxin III-deficiency Sensitizes Macrophages to Oxidative Stress
1 Obstetrics and Gynecology Center, Tsinghua University Second Hospital, Beijing 100049 China
2 Department of Cell Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575 Japan
3 Department of Experimental Immunology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575 Japan
*To whom correspondence should be addressed: Lianqin Li, Obstetrics and Gynecology Center, Tsinghua University Second Hospital 5 Shijingshan Road, Shijingshan-district, Beijing 100049 China Tel: +86-10-87002811 Fax: +86-10-88257362 E-mail: lilq2005{at}126.com
Received January 11, 2009; Accepted January 13, 2009
| Abstract |
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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 tumor necrosis factor alpha (TNF-
) in mouse bone marrow-derived macrophages. LPS stimulation induced transient increase of ROS production and augmentation of TNF-
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.
Key Words: lipopolysaccharide, macrophage, mouse, peroxiredoxin III, reactive oxygen species