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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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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/53702

Title: Oxidative stress induction of DJ-1 protein in reactive astrocytes scavenges free radicals and reduces cell injury.
Authors: Yanagida, Takashi Browse this author
Tsushima, Jun Browse this author
Kitamura, Yoshihisa Browse this author →KAKEN DB
Yanagisawa, Daijiro Browse this author
Takata, Kazuyuki Browse this author →KAKEN DB
Shibaike, Tomonori Browse this author
Yamamoto, Atsuko Browse this author
Taniguchi, Takashi Browse this author →KAKEN DB
Yasui, Hiroyuki Browse this author →KAKEN DB
Taira, Takahiro Browse this author →KAKEN DB
Morikawa, Shigehiro Browse this author →KAKEN DB
Inubushi, Toshihiro Browse this author
Tooyama, Ikuo Browse this author →KAKEN DB
Ariga, Hiroyoshi Browse this author →KAKEN DB
Keywords: DJ-1
release
astrocytes
focal ischemia
oxidative stress sensor
neuroprotection
Issue Date: Jan-2009
Publisher: Hindawi Pub.
Journal Title: Oxidative medicine and cellular longevity
Volume: 2
Issue: 1
Start Page: 36
End Page: 42
Publisher DOI: 10.4161/oxim.2.1.7985
PMID: 20046643
Abstract: 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.
Type: article
URI: http://hdl.handle.net/2115/53702
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 有賀 寛芳

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