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Dual functionality of myeloperoxidase in rotenone-exposed brain-resident immune cells

Title
Dual functionality of myeloperoxidase in rotenone-exposed brain-resident immune cells
Authors
Chang C.Y.Song M.J.Jeon S.-B.Yoon H.J.Lee D.K.Kim I.-H.Suk K.Choi D.-K.Park E.J.
Ewha Authors
이대기
SCOPUS Author ID
이대기scopus
Issue Date
2011
Journal Title
American Journal of Pathology
ISSN
0002-9440JCR Link
Citation
vol. 179, no. 2, pp. 964 - 979
Indexed
SCI; SCIE; SCOPUS WOS scopus
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.
DOI
10.1016/j.ajpath.2011.04.033
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자연과학대학 > 생명과학전공 > Journal papers
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