1. Inhibitory role of peroxiredoxin II (Prx II) on cellular senescence
- Author
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Jin Man Kim, Ying-Hao Han, Hyun-Sun Kim, Eun-Yi Moon, Sang-Keun Kim, and Dae-Yeul Yu
- Subjects
MAPK/ERK pathway ,Senescence ,Aging ,p38 mitogen-activated protein kinases ,Biophysics ,Biology ,Biochemistry ,Mice ,Peroxiredoxin II ,Structural Biology ,Genetics ,Extracellular ,Animals ,Molecular Biology ,Cells, Cultured ,Cellular Senescence ,chemistry.chemical_classification ,Mice, Knockout ,Reactive oxygen species ,Kinase ,Cell Cycle ,Wild type ,Cell Biology ,Hydrogen Peroxide ,Peroxiredoxins ,Fibroblasts ,Oxidants ,Molecular biology ,Acetylcysteine ,chemistry ,Peroxidases ,embryonic structures ,Peroxiredoxin ,Reactive Oxygen Species - Abstract
Reactive oxygen species (ROS) were generated in all oxygen-utilizing organisms. Peroxiredoxin II (Prx II) as one of antioxidant enzymes may play a protective role against the oxidative damage caused by ROS. In order to define the role of Prx II in organismal aging, we evaluated cellular senescence in Prx II(-/-) mouse embryonic fibroblast (MEF). As compared to wild type MEF, cellular senescence was accelerated in Prx II(-/-) MEF. Senescence-associated (SA)-beta-galactosidase (Gal)-positive cell formation was about 30% higher in Prx II(-/-) MEF. N-Acetyl-l-cysteine (NAC) treatment attenuated SA-beta-Gal-positive cell formation. Prx II(-/-) MEF exhibited the higher G2/M (41%) and lower S (1.6%) phase cells as compared to 24% and 7.3% [corrected] in wild type MEF, respectively. A high increase in the p16 and a slight increase in the p21 and p53 levels were detected in PrxII(-/-) MEF cells. The cellular senescence of Prx II(-/-) MEF was correlated with the organismal aging of Prx II(-/-) mouse skin. While extracellular signal-regulated kinase (ERK) and p38 activation was detected in Prx II(-/-) MEF, ERK and c-Jun N-terminal kinase (JNK) activation was detected in Prx II(-/-) skin. These results suggest that Prx II may function as an enzymatic antioxidant to prevent cellular senescence and skin aging.
- Published
- 2005