| First Author | Park YH | Year | 2017 |
| Journal | BMB Rep | Volume | 50 |
| Issue | 10 | Pages | 528-533 |
| PubMed ID | 28893373 | Mgi Jnum | J:294803 |
| Mgi Id | MGI:6458612 | Doi | 10.5483/bmbrep.2017.50.10.121 |
| Citation | Park YH, et al. (2017) Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence. BMB Rep 50(10):528-533 |
| abstractText | 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-beta-galactosidase (SA-beta-gal) activity in a variety of tissues. Increased ROS levels and SA-beta-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]. |
