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Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence
Young-Ho Park2,3,7,#, Hyun-Sun Kim1,#, Jong-Hee Lee2,#, Seon-A Choi2,3, Jin-Man Kim4, Goo Taeg Oh5, Sang Won Kang6, Sun-Uk Kim2,3,7,*, Dae-Yeul Yu1,7
1Disease Model Research Laboratory, Genome Editing Research Center and 2National Primate Research Center and 3Futuristic Animal Resource & Research Center, Korea Research Institute of Bioscience and Biotechnology,
4College of Medicine, Chungnam National University,
56Department of Life Sciences and Immune and Vascular Cell Network Research Center and 6Department of Life Sciences and Cell Homeostasis Research Center, Ewha Womans University,
7Department of Functional Genomics, University of Science and Technology
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-モ-galactosidase (SA-モ-gal) activity in a variety of tissues. Increased ROS levels and SA-モ-gal activity in Prx I-/- MEFs and reduction with a chemical antioxidant further supported an essential role for 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.
Abstract, Accepted Manuscript(in press) [Submitted on July 7, 2017, Accepted on September 12, 2017]
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