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

• Published in: BMB reports Vol. 50; no. 10; pp. 528 - 533
• Main 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
• Format: Journal Article
• Language: English
• Published: Korea (South) Korean Society for Biochemistry and Molecular Biology 01.10.2017; 생화학분자생물학회
• Subjects: Animals; Antioxidants - metabolism; Cells, Cultured; Cellular Senescence - physiology; Fibroblasts - metabolism; Fibroblasts - physiology; Homeodomain Proteins - metabolism; Homeodomain Proteins - physiology; Mice; Oxidation-Reduction; Oxidative Stress; Peroxiredoxins - genetics; Peroxiredoxins - metabolism; Peroxiredoxins - physiology; Reactive Oxygen Species - metabolism; Up-Regulation; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2017.50.10.121

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].