Effects of Tat-DJ-1 Protein on Oxidative Stress-Induced Neuronal Cell Death in Parkinson Disease Mouse Model

被引:0
|
作者
Jeong, Hoon Jae [1 ,2 ]
Kim, Dae Won [1 ,2 ]
Park, Jinseu [1 ,2 ]
Eum, Won Sik [1 ,2 ]
Choi, Soo Young [1 ,2 ]
机构
[1] Hallym Univ, Dept Biomed Sci, Chunchon 200702, South Korea
[2] Hallym Univ, Res Inst Biosci & Biotechnol, Chunchon 200702, South Korea
来源
BIOSCIENCE, BIOCHEMISTRY AND BIOINFORMATICS | 2011年 / 5卷
基金
新加坡国家研究基金会;
关键词
Antioxidant; Parkinson disease; Protein transduction; ROS; Tat-DJ-1; TRANSDUCTION;
D O I
暂无
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Reactive oxygen species (ROS) is known represent one of the principal factors that cause cell death. The scavenging of ROS is essential for cell survival and ROS plays critical roles in the pathogenesis of Parkinson disease (PD). PD is a neurodegenerative disorder characterized by selective loss of dopaminergic neurons. Although DJ-1 protein, known to resistance ROS in dopaminergic neurons, its mechanism has not been elucidate yet. Thus, we investigated the protective effects of DJ-1 protein against SH-SY5Y cells and PD mouse model using cell-permeable Tat-DJ-1 fusion protein. Tat-DJ-1 protein transduced into the cells and shows protective effect on 6-hydroxydopamine (6-OHDA)-induced neuronal cell death by reduced the ROS. In the 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP)-induced PD mouse models, Tat DJ-1 protein protects against dopaminergic neuronal cell death. These results suggest that Tat-DJ-1 protein provides a potential strategy for therapeutic delivery in various human diseases including PD.
引用
收藏
页码:165 / 169
页数:5
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