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Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence
- Title
- Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence
- Authors
- Park, Young-Ho; Kim, Hyun-Sun; Lee, Jong-Hee; Choi, Seon-A; Kim, Jin-Man; Oh, Goo Taeg; Kang, Sang Won; Kim, Sun-Uk; Yu, Dae-Yeul
- Ewha Authors
- 강상원; 오구택
- SCOPUS Author ID
- 강상원; 오구택
- Issue Date
- 2017
- Journal Title
- BMB REPORTS
- ISSN
- 1976-6696
1976-670X
- Citation
- BMB REPORTS vol. 50, no. 10, pp. 528 - 533
- Keywords
- Antioxidant enzyme; Cellular senescence; Oxidative stress; p16(INK4a); Peroxiredoxin
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY &
MOLECULAR BIOLOGY
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Article
- 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.
- DOI
- 10.5483/BMBRep.2017.50.10.121
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
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