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Nox4-dependent H2O2 production contributes to chronic glutamate toxicity in primary cortical neurons

Title
Nox4-dependent H2O2 production contributes to chronic glutamate toxicity in primary cortical neurons
Authors
Ha J.S.Lee J.E.Lee J.-R.Lee C.-S.Maeng J.-S.Bae Y.S.Kwon K.-S.Park S.S.
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2010
Journal Title
Experimental Cell Research
ISSN
0014-4827JCR Link
Citation
vol. 316, no. 10, pp. 1651 - 1661
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Reactive oxygen species (ROS) can trigger neuronal cell death and has been implicated in a variety of neurodegenerative diseases as well as brain ischemia. Here, we demonstrate that chronic (but not acute) glutamate toxicity in primary cortical neuronal cultures is associated with hydrogen peroxide (H2O2) accumulation in the culture medium and that neurotoxicity can be eliminated by external catalase treatment. Neuronal cultures in Ca2+-free medium or treated with BAPTA showed reduced glutamate-induced H2O2 generation, indicating that H2O2 generation is Ca2+-dependent. Pharmacological and genetic approaches revealed that NADPH oxidase plays a role in glutamate-induced H2O2 generation and that activation of NMDA and AMPA receptors is involved in this H2O2 generation. The Nox4 siRNA reduced NMDA-induced H2O2 production by 54% and cytotoxicity in parallel, suggesting that Nox4-containing NADPH oxidase functions NMDA receptor-mediated H2O2 production resulting in neurotoxicity. These findings suggest that the modulation of NADPH oxidase can be used as a new therapeutic strategy for glutamate-induced neuronal diseases. © 2010 Elsevier Inc.
DOI
10.1016/j.yexcr.2010.03.021
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자연과학대학 > 생명과학전공 > Journal papers
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