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Title
  • Oxidative stress induction of DJ-1 protein in reactive astrocytes scavenges free radicals and reduces cell injury.
Creator

Yanagida, Takashi

Tsushima, Jun

Kitamura, Yoshihisa

Yanagisawa, Daijiro

Takata, Kazuyuki

Shibaike, Tomonori

Yamamoto, Atsuko

Taniguchi, Takashi

Yasui, Hiroyuki

Taira, Takahiro

Morikawa, Shigehiro

Inubushi, Toshihiro

Tooyama, Ikuo

Ariga, Hiroyoshi

Subject
  • Other DJ-1
  • Other release
  • Other astrocytes
  • Other focal ischemia
  • Other oxidative stress sensor
  • Other neuroprotection
  • NDC 499
  • MeSH Animals
  • MeSH Astrocytes/metabolism
  • MeSH Brain Ischemia/metabolism
  • MeSH Brain Ischemia/pathology
  • MeSH Cell Line
  • MeSH Electron Spin Resonance Spectroscopy
  • MeSH Humans
  • MeSH Hydrogen Peroxide/pharmacology
  • MeSH Hydroxyl Radical/metabolism
  • MeSH Infarction, Middle Cerebral Artery/metabolism
  • MeSH Infarction, Middle Cerebral Artery/pathology
  • MeSH Microtubule-Associated Proteins/genetics
  • MeSH Microtubule-Associated Proteins/metabolism
  • MeSH Oxidative Stress
  • MeSH Rats
  • MeSH Recombinant Fusion Proteins/pharmacology
  • MeSH Recombinant Proteins/genetics
  • MeSH Recombinant Proteins/metabolism
Description
Other
  • 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.
PublisherHindawi Pub.
Date Issued 2009-01
Languageeng
NIItypejournal article
VersiontypeVoR
Identifier URI http://hdl.handle.net/2115/53702
Relation
  • isIdenticalTo PMID 20046643
  • isIdenticalTo DOI https://doi.org/10.4161/oxim.2.1.7985
Journal
    • ISSN 1942-0994
    • Oxidative medicine and cellular longevity
    2(1), 36-42
File
Oaidate2017-10-15T15:00:00Z