Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence
2017
Park, Y.H., Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea | Kim, H.S., Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea | Lee, J.H., Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea | Choi, S.A., Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea | Kim, J.M., Chungnam National University, Daejeon, Republic of Korea | Oh, G.T., Ewha Womans University, Seoul, Republic of Korea | Kang, S.W., Ewha Womans University, Seoul, Republic of Korea | Kim, S.U., Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea | Yu, D.Y., Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea
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.
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