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http://dx.doi.org/10.5483/BMBRep.2017.50.10.121

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)
Publication Information
BMB Reports / v.50, no.10, 2017 , pp. 528-533 More about this Journal
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
Antioxidant enzyme; Cellular senescence; Oxidative stress; $p16^{INK4a}$; Peroxiredoxin;
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Times Cited By KSCI : 2  (Citation Analysis)
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