Inhibitory role of peroxiredoxin II (Prx II) on cellular senescence

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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)‐β‐galactosidase (Gal)‐positive cell formation was about 30% higher in Prx II−/− MEF. N‐Acetyl‐l‐cysteine (NAC) treatment attenuated SA‐β‐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 7.4% 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.