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Peroxiredoxin I is a ROS/p38 MAPK-dependent inducible antioxidant that regulates NF-κB-mediated iNOS induction and microglial activation

Title
Peroxiredoxin I is a ROS/p38 MAPK-dependent inducible antioxidant that regulates NF-κB-mediated iNOS induction and microglial activation
Authors
Kim S.-U.Park Y.-H.Min J.-S.Sun H.-N.Han Y.-H.Hua J.-M.Lee T.-H.Lee S.-R.Chang K.-T.Kang S.W.Kim J.-M.Yu D.-Y.Lee S.-H.Lee D.-S.
Ewha Authors
강상원
SCOPUS Author ID
강상원scopus
Issue Date
2013
Journal Title
Journal of Neuroimmunology
ISSN
0165-5728JCR Link
Citation
vol. 259, no. 41276, pp. 26 - 36
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Reactive oxygen species (ROS) function as modulators of pro-inflammatory processes in microglia-associated neurodegenerative diseases.However, little is known about the involvement of specific antioxidants in regulating the microglial redox status. Here, we demonstrated that peroxiredoxin (Prx) I activity was induced by lipopolysaccharide (LPS), but not paraquat and hydrogen peroxide, through activation of the ROS/p38 MAPK signal pathway, and participated in alleviating the microglial activation and generation of nitric oxide (NO). Interestingly, a null mutation of Prx I accelerated NF-κB-mediated iNOS induction and subsequent NO secretion in LPS-stimulated microglia. Furthermore, F4/80 expression as microglial activation marker was notably up-regulated in primary cultures of microglia, hippocampal sections, and cerebral cortex of 15-month-old Prx I-/- mouse.Taken together, the results of our study indicated that Prx I is an antioxidant that is up-regulated in a ROS/p38 MAPK-dependent manner and governs the progression of neuroinflammation by suppressing microglial activation. In addition, Prx I deficiency increased the nuclear translocation of NF-κB mediated-iNOS induction as pro-inflammatory mediators.The findings of our work suggest possible strategies for developing novel therapies to treat inflammation-associated degenerative neurological diseases by targeting the induction of Prx I in microglial cells. © 2013 Elsevier B.V.
DOI
10.1016/j.jneuroim.2013.03.006
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자연과학대학 > 생명과학전공 > Journal papers
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