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DOI QR Code

Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence

  • Park, Young-Ho (National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology) ;
  • Kim, Hyun-Sun (Disease Model Research Laboratory, Genome Editing Research Center, Korea Research Institute of Bioscience and Biotechnology) ;
  • Lee, Jong-Hee (National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology) ;
  • Cho, Seon-A (National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology) ;
  • Kim, Jin-Man (College of Medicine, Chungnam National University) ;
  • Oh, Goo Taeg (Department of Life Sciences and Immune and Vascular Cell Network Research Center, Ewha Womans University) ;
  • Kang, Sang Won (Department of Life Sciences and Cell Homeostasis Research Center, Ewha Womans University) ;
  • Kim, Sun-Uk (National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology) ;
  • Yu, Dae-Yeul (Disease Model Research Laboratory, Genome Editing Research Center, Korea Research Institute of Bioscience and Biotechnology)
  • Received : 2017.07.07
  • Accepted : 2017.09.12
  • Published : 2017.10.31

Abstract

Peroxiredoxin I (Prx I) plays an important role as a reactive oxygen species (ROS) scavenger in protecting and maintaining cellular homeostasis; however, the underlying mechanisms are not well understood. Here, we identified a critical role of Prx I in protecting cells against ROS-mediated cellular senescence by suppression of $p16^{INK4a}$ expression. Compared to wild-type mouse embryonic fibroblasts (WT-MEFs), Prx $I^{-/-}$ MEFs exhibited senescence-associated phenotypes. Moreover, the aged Prx $I^{-/-}$ mice showed an increased number of cells with senescence associated-${\beta}$-galactosidase (SA-${\beta}$-gal) activity in a variety of tissues. Increased ROS levels and SA-${\beta}$-gal activity, and reduction of chemical antioxidant in Prx $I^{-/-}$ MEF further supported an essential role of Prx I peroxidase activity in cellular senescence that is mediated by oxidative stress. The up-regulation of $p16^{INK4a}$ expression in Prx $I^{-/-}$ and suppression by overexpression of Prx I indicate that Prx I possibly modulate cellular senescence through $ROS/p16^{INK4a}$ pathway.

Keywords

References

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