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タイトル
  • en Oxidative stress induction of DJ-1 protein in reactive astrocytes scavenges free radicals and reduces cell injury.
作成者
アクセス権 open access
主題
  • Other en DJ-1
  • Other en release
  • Other en astrocytes
  • Other en focal ischemia
  • Other en oxidative stress sensor
  • Other en neuroprotection
  • MeSH en Animals
  • MeSH en Astrocytes/metabolism
  • MeSH en Brain Ischemia/metabolism
  • MeSH en Brain Ischemia/pathology
  • MeSH en Cell Line
  • MeSH en Electron Spin Resonance Spectroscopy
  • MeSH en Humans
  • MeSH en Hydrogen Peroxide/pharmacology
  • MeSH en Hydroxyl Radical/metabolism
  • MeSH en Infarction, Middle Cerebral Artery/metabolism
  • MeSH en Infarction, Middle Cerebral Artery/pathology
  • MeSH en Microtubule-Associated Proteins/genetics
  • MeSH en Microtubule-Associated Proteins/metabolism
  • MeSH en Oxidative Stress
  • MeSH en Rats
  • MeSH en Recombinant Fusion Proteins/pharmacology
  • MeSH en Recombinant Proteins/genetics
  • MeSH en Recombinant Proteins/metabolism
  • NDC 499
内容注記
  • Abstract en 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.
出版者 en Hindawi Pub.
日付
    Issued2009-01
言語
  • eng
資源タイプ journal article
出版タイプ VoR
資源識別子 HDL http://hdl.handle.net/2115/53702
関連
  • isIdenticalTo DOI https://doi.org/10.4161/oxim.2.1.7985
  • PMID 20046643
収録誌情報
    • PISSN 1942-0994
      • en Oxidative medicine and cellular longevity
      • 2 1 開始ページ36 終了ページ42
ファイル
コンテンツ更新日時 2023-07-26