Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence
- 주제(키워드) Antioxidant enzyme , Cellular senescence , Oxidative stress , p16INK4a , Peroxiredoxin
- 등재 SCIE, SCOPUS, KCI등재
- 발행기관 The Biochemical Society of the Republic of Korea
- 발행년도 2017
- URI http://www.dcollection.net/handler/ewha/000000155952
- 본문언어 영어
- Published As http://dx.doi.org/10.5483/BMBRep.2017.50.10.121
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
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. © 2017 by the The Korean Society for Biochemistry and Molecular Biology.
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