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首页> 美国卫生研究院文献>PLoS Clinical Trials >Overexpression of Parkin Ameliorates Dopaminergic Neurodegeneration Induced by 1- Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice
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Overexpression of Parkin Ameliorates Dopaminergic Neurodegeneration Induced by 1- Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice

机译：1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的小鼠帕金过表达改善多巴胺能神经变性

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摘要

Mutations in the parkin gene are currently thought to be the most common cause of recessive familial Parkinsonism. Parkin functions as an E3 ligase to regulate protein turnover, and its function in mitochondrial quality control has been reported recently. Overexpression of parkin has been found to prevent neuronal degeneration under various conditions both in vivo and in vitro. Here, we generated a transgenic mouse model in which expression of wild type parkin was driven by neuron-specific enolase (NSE) promoter. We reported that both young and old parkin transgenic mice exhibited less reduction of striatal TH protein and number of TH positive neurons in the substantia nigra induced by 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP), compared to wild type littermates. MPTP-induced mitochondrial impairment in the substantia nigra was improved in young parkin transgenic mice. Decreased striatal α-synuclein was demonstrated in old parkin transgenic mice. These results provide reliable evidence from the transgenic mouse model for parkin that overexpression of parkin may attenuate dopaminergic neurodegeneration induced by MPTP through protection of mitochondria and reduction of α-synuclein in the nigrostriatal pathway.
机译：目前认为，帕金基因的突变是隐性家族性帕金森病的最常见原因。帕金作为E3连接酶来调节蛋白质更新，最近在线粒体质量控制中已有报道。已经发现，在体内和体外的各种条件下，Parkin的过度表达都可以防止神经元变性。在这里，我们生成了一个转基因小鼠模型，其中野生型帕金菌的表达由神经元特异性烯醇化酶（NSE）启动子驱动。我们报道，无论是年轻还是老的Parkin转基因小鼠，在1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的黑质中，纹状体TH蛋白的减少和TH阳性神经元的数量减少，与野生型同窝仔相比。在年轻的帕金转基因小鼠中，MPTP诱导的黑质线粒体损伤得到改善。在老帕金转基因小鼠中证实纹状体α-突触核蛋白减少。这些结果提供了来自Parkin转基因小鼠模型的可靠证据，表明Parkin的过表达可能通过保护线粒体和减少黑质纹状体途径中的α-突触核蛋白而减弱了MPTP诱导的多巴胺能神经变性。

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