TY - JOUR
T1 - DJ-1 has a role in antioxidative stress to prevent cell death
AU - Taira, Takahiro
AU - Saito, Yoshiro
AU - Niki, Takeshi
AU - Iguchi-Ariga, Sanae M.M.
AU - Takahashi, Kazuhiko
AU - Ariga, Hiroyoshi
PY - 2004/2
Y1 - 2004/2
N2 - Deletion and point (L166P) mutations of DJ-1 have recently been shown to be responsible for the onset of familial Parkinson's disease (PD, PARK7). The aim of this study was to determine the role of DJ-1 in PD. We first found that DJ-1 eliminated hydrogen peroxide in vitro by oxidizing itself. We then found that DJ-1 knockdown by short interfering RNA rendered SH-SY5Y neuroblastoma cells susceptible to hydrogen peroxide-, MPP+- or 6-hydroxydopamine-induced cell death and that cells harbouring mutant forms of DJ-1, including L166P, became susceptible to death in parallel with the loss of oxidized forms of DJ-1. These results clearly showed that DJ-1 has a role in the antioxidative stress reaction and that mutations of DJ-1 lead to cell death, which is observed in PD.
AB - Deletion and point (L166P) mutations of DJ-1 have recently been shown to be responsible for the onset of familial Parkinson's disease (PD, PARK7). The aim of this study was to determine the role of DJ-1 in PD. We first found that DJ-1 eliminated hydrogen peroxide in vitro by oxidizing itself. We then found that DJ-1 knockdown by short interfering RNA rendered SH-SY5Y neuroblastoma cells susceptible to hydrogen peroxide-, MPP+- or 6-hydroxydopamine-induced cell death and that cells harbouring mutant forms of DJ-1, including L166P, became susceptible to death in parallel with the loss of oxidized forms of DJ-1. These results clearly showed that DJ-1 has a role in the antioxidative stress reaction and that mutations of DJ-1 lead to cell death, which is observed in PD.
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U2 - 10.1038/sj.embor.7400074
DO - 10.1038/sj.embor.7400074
M3 - Article
C2 - 14749723
AN - SCOPUS:1642527499
VL - 5
SP - 213
EP - 218
JO - EMBO Reports
JF - EMBO Reports
SN - 1469-221X
IS - 2
ER -