Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이대기 | * |
dc.date.accessioned | 2016-08-28T12:08:40Z | - |
dc.date.available | 2016-08-28T12:08:40Z | - |
dc.date.issued | 2011 | * |
dc.identifier.issn | 0002-9440 | * |
dc.identifier.other | OAK-8277 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222201 | - |
dc.description.abstract | Rotenone exposure has emerged as an environmental risk factor for inflammation-associated neurodegenerative diseases. However, the underlying mechanisms responsible for the harmful effects of rotenone in the brain remain poorly understood. Herein, we report that myeloperoxidase (MPO) may have a potential regulatory role in rotenone-exposed brain-resident immune cells. We show that microglia, unlike neurons, do not undergo death; instead, they exhibit distinctive activated properties under rotenone-exposed conditions. Once activated by rotenone, microglia show increased production of reactive oxygen species, particularly HOCl. Notably, MPO, an HOCl-producing enzyme that is undetectable under normal conditions, is significantly increased after exposure to rotenone. MPO-exposed glial cells also display characteristics of activated cells, producing proinflammatory cytokines and increasing their phagocytic activity. Interestingly, our studies with MPO inhibitors and MPO-knockout mice reveal that MPO deficiency potentiates, rather than inhibits, the rotenone-induced activated state of glia and promotes glial cell death. Furthermore, rotenone-triggered neuronal injury was more apparent in co-cultures with glial cells from Mpo -/- mice than in those from wild-type mice. Collectively, our data provide evidence that MPO has dual functionality under rotenone-exposed conditions, playing a critical regulatory role in modulating pathological and protective events in the brain. © 2011 American Society for Investigative Pathology. | * |
dc.language | English | * |
dc.title | Dual functionality of myeloperoxidase in rotenone-exposed brain-resident immune cells | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 179 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 964 | * |
dc.relation.lastpage | 979 | * |
dc.relation.journaltitle | American Journal of Pathology | * |
dc.identifier.doi | 10.1016/j.ajpath.2011.04.033 | * |
dc.identifier.wosid | WOS:000298307200041 | * |
dc.identifier.scopusid | 2-s2.0-80052514464 | * |
dc.author.google | Chang C.Y. | * |
dc.author.google | Song M.J. | * |
dc.author.google | Jeon S.-B. | * |
dc.author.google | Yoon H.J. | * |
dc.author.google | Lee D.K. | * |
dc.author.google | Kim I.-H. | * |
dc.author.google | Suk K. | * |
dc.author.google | Choi D.-K. | * |
dc.author.google | Park E.J. | * |
dc.contributor.scopusid | 이대기(37047040400) | * |
dc.date.modifydate | 20231120165418 | * |