DJ-1 has a role in antioxidative stress to prevent cell death
DJ-1 has a role in antioxidative stress to prevent cell death
复制标题
DOI：
10.1038/sj.embor.7400074
复制
发表时间：
2004-02-01
期刊：
影响因子：
7.7
通讯作者：
Ariga, H
中科院分区：
文献类型：
--
作者：
Taira, T;Saito, Y;Ariga, H
DJ-1的缺失和点（L166 P）突变最近已被证明是家族性帕金森病（PD，PARK 7）发病的原因。本研究的目的是确定DJ-1在PD中的作用。我们首次发现DJ-1在体外通过氧化自身消除过氧化氢。然后，我们发现，短干扰RNA敲低DJ-1使SH-SY 5 Y神经母细胞瘤细胞对过氧化氢、MPP+或6-羟基多巴胺诱导的细胞死亡敏感，并且携带DJ-1突变形式（包括L166 P）的细胞在失去氧化形式的DJ-1的同时变得对死亡敏感。这些结果清楚地表明，DJ-1在抗氧化应激反应中具有作用，并且DJ-1的突变导致细胞死亡，这在PD中观察到。
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.