Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 강상원 | * |
dc.date.accessioned | 2016-08-28T10:08:05Z | - |
dc.date.available | 2016-08-28T10:08:05Z | - |
dc.date.issued | 2013 | * |
dc.identifier.issn | 0165-5728 | * |
dc.identifier.other | OAK-10155 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/223783 | - |
dc.description.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. | * |
dc.language | English | * |
dc.title | Peroxiredoxin I is a ROS/p38 MAPK-dependent inducible antioxidant that regulates NF-κB-mediated iNOS induction and microglial activation | * |
dc.type | Article | * |
dc.relation.issue | 41276 | * |
dc.relation.volume | 259 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 26 | * |
dc.relation.lastpage | 36 | * |
dc.relation.journaltitle | Journal of Neuroimmunology | * |
dc.identifier.doi | 10.1016/j.jneuroim.2013.03.006 | * |
dc.identifier.wosid | WOS:000319848100004 | * |
dc.identifier.scopusid | 2-s2.0-84877596486 | * |
dc.author.google | Kim S.-U. | * |
dc.author.google | Park Y.-H. | * |
dc.author.google | Min J.-S. | * |
dc.author.google | Sun H.-N. | * |
dc.author.google | Han Y.-H. | * |
dc.author.google | Hua J.-M. | * |
dc.author.google | Lee T.-H. | * |
dc.author.google | Lee S.-R. | * |
dc.author.google | Chang K.-T. | * |
dc.author.google | Kang S.W. | * |
dc.author.google | Kim J.-M. | * |
dc.author.google | Yu D.-Y. | * |
dc.author.google | Lee S.-H. | * |
dc.author.google | Lee D.-S. | * |
dc.contributor.scopusid | 강상원(55731433900) | * |
dc.date.modifydate | 20240118155300 | * |