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 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 language | English |
|---|---|
| Pages (from-to) | 528-533 |
| Number of pages | 6 |
| Journal | BMB Reports |
| Volume | 50 |
| Issue number | 10 |
| DOIs | |
| State | Published - 2017 |
Bibliographical note
Publisher Copyright:© 2017 by the The Korean Society for Biochemistry and Molecular Biology.
Keywords
- Antioxidant enzyme
- Cellular senescence
- Oxidative stress
- Peroxiredoxin
- p16INK4a