Title |
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Oxidative stress induction of DJ-1 protein in reactive astrocytes scavenges free radicals and reduces cell injury.
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Creator |
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Accessrights |
open access |
Subject |
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Other
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DJ-1
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Other
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release
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Other
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astrocytes
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Other
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focal ischemia
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Other
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oxidative stress sensor
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Other
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neuroprotection
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MeSH
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Animals
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MeSH
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Astrocytes/metabolism
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MeSH
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Brain Ischemia/metabolism
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MeSH
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Brain Ischemia/pathology
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MeSH
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Cell Line
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MeSH
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Electron Spin Resonance Spectroscopy
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MeSH
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Humans
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MeSH
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Hydrogen Peroxide/pharmacology
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MeSH
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Hydroxyl Radical/metabolism
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MeSH
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Infarction, Middle Cerebral Artery/metabolism
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MeSH
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Infarction, Middle Cerebral Artery/pathology
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MeSH
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Microtubule-Associated Proteins/genetics
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MeSH
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Microtubule-Associated Proteins/metabolism
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MeSH
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Oxidative Stress
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MeSH
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Rats
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MeSH
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Recombinant Fusion Proteins/pharmacology
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MeSH
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Recombinant Proteins/genetics
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MeSH
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Recombinant Proteins/metabolism
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NDC
499
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Description |
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Abstract
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Astrocytes, one of the predominant types of glial cells, function as both supportive and metabolic cells for the brain. Under cerebral ischemia/reperfusion-induced oxidative conditions, astrocytes accumulate and activate in the ischemic region. DJ-1 has recently been shown to be a sensor of oxidative stress in living cells. However, the function of astrocytic DJ-1 is still unknown. In the present study, to clarify the effect of astrocytic DJ-1 protein under massive oxidative insult, we used a focal ischemic rat model that had been subjected to middle cerebral artery occlusion (MCAO) and reperfusion. We then investigated changes in the distribution of DJ-1 in astrocytes, DJ-1 release from cultured astrocytes, and the effects of recombinant DJ-1 protein on hydrogen peroxide (H(2)O(2))-induced death in normal and DJ-1-knockdown SH-SY5Y cells and on in vitro scavenging of hydroxyl radicals ((*)OH) by electron spin resonance spectrometry. At 24 h after 2-h MCAO and reperfusion, an infarct lesion was markedly observed using magnetic resonance imaging and 2,3,5-triphenyltetrazolium chloride staining. In addition, reactive astrocytes enhanced DJ-1 expression in the penumbral zone of the ischemic core and that DJ-1 protein was extracellularly released from astrocytes by H2O2 in in vitro primary cultures. Although DJ-1-knockdown SH-SY5Y cells were markedly vulnerable to oxidative stress, treatment with glutathione S-transferase-tagged recombinant human DJ-1 protein (GST-DJ-1) significantly inhibited H(2)O(2)-induced cell death. In addition, GST-DJ-1 protein directly scavenged (*)OH. These results suggest that oxidative stress induces the release of astrocytic DJ-1 protein, which may contribute to astrocyte-mediated neuroprotection.
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Publisher |
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Hindawi Pub.
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Date |
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Language |
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Resource Type |
journal article |
Version Type |
VoR |
Identifier |
HDL
http://hdl.handle.net/2115/53702
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Relation |
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isIdenticalTo
DOI
https://doi.org/10.4161/oxim.2.1.7985
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PMID
20046643
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Journal |
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Oxidative medicine and cellular longevity
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Volume Number2
Issue Number1
Page Start36
Page End42
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File |
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Oaidate |
2023-07-26 |