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BMB Rep. 2017 Oct;50(10):528-533.

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

Author information

1
National Primate Research Center, and Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Korea; Department of Functional Genomics, University of Science and Technology, Daejeon 34113, Korea.
2
Disease Model Research Laboratory, Genome Editing Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
3
National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Korea.
4
National Primate Research Center, and Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Korea.
5
College of Medicine, Chungnam National University, Daejeon 35015, Korea.
6
Department of Life Sciences and Immune and Vascular Cell Network Research Center, Ewha Womans University, Seoul 03760, Korea.
7
Department of Life Sciences and Cell Homeostasis Research Center, Ewha Womans University, Seoul 03760, Korea.
8
Disease Model Research Laboratory, Genome Editing Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea; Department of Functional Genomics, University of Science and Technology, Daejeon 34113, Korea.

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 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 further in Prx I-/- MEF 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. [BMB Reports 2017; 50(10): 528-533].

PMID:
28893373
PMCID:
PMC5683823
DOI:
10.5483/bmbrep.2017.50.10.121
[Indexed for MEDLINE]
Free PMC Article

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