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

Young Ho Park, Hyun Sun Kim, Jong Hee Lee, Seon A. Choi, Jin Man Kim, Goo Taeg Oh, Sang Won Kang, Sun Uk Kim, Dae Yeul Yu

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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 p16INK4a 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-β-galactosidase (SA-β-gal) activity in a variety of tissues. Increased ROS levels and SA-β-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 p16INK4a expression in Prx I-/- and suppression by overexpression of Prx I indicate that Prx I possibly modulate cellular senescence through ROS/p16INK4a pathway.

Original languageEnglish
Pages (from-to)528-533
Number of pages6
JournalBMB Reports
Issue number10
StatePublished - 2017

Bibliographical note

Publisher Copyright:
© 2017 by the The Korean Society for Biochemistry and Molecular Biology.


  • Antioxidant enzyme
  • Cellular senescence
  • Oxidative stress
  • Peroxiredoxin
  • p16INK4a


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