铜- atp酶ATP7A在小鼠神经细胞中的表达和定位

J. Cheng, P. Guo, Z. Wang, L. Sun
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引用次数: 0

摘要

铜是人体必需的微量营养素,其氧化还原特性在神经系统中起着重要的生物化学作用。Menkes病(一种由ATP7A铜转运体突变引起的x连锁神经退行性疾病)证明了它的重要性,表明ATP7A与神经系统的发育有关。为了研究ATP7A在神经元发育中的调控作用,我们分析了体外培养的C57BL/6小鼠神经干细胞、星形胶质细胞和海马神经元中ATP7A mRNA、蛋白的表达和定位。结果表明,ATP7A在NSC、星形胶质细胞和海马神经元中的表达逐渐降低。在三种细胞中,ATP7A的荧光信号位于细胞核和质膜之间。由此可见,ATP7A可能参与了神经元和星形胶质细胞的发育。这项研究可能有助于了解ATP7A基因突变引起的铜代谢疾病的严重神经变性特征。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression and localization of the copper-ATPase ATP7A in mice neural cells
Abstract Copper is an essential micronutrient as its redox properties play a significant biochemistry role in the nervous system. Its essentiality is evidenced by Menkes disease (MD), an X-linked neurodegenerative disease caused by mutations in the ATP7A copper transporter, showing that ATP7A is concerned with the development of the nervous system. To investigate the regulation of ATP7A in the development of neurons, we analyzed the expression of the mRNA, protein and the localization of ATP7A in C57BL/6 mice neural stem cells (NSCs), astrocytes and hippocampal neurons cultured in vitro. The results indicated that ATP7A expression was decreased stepwise in NSC, astrocytes and hippocampal neurons. The fluorescent signals of ATP7A were located between the nucleus and plasma membrane in the three kinds of cells. It can be concluded that ATP7A might be involved in the development of neurons and astrocytes. This research may contribute to knowledge about the severe neurodegeneration characteristic of copper-metabolic diseases caused by mutations in the ATP7A gene.
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来源期刊
Italian Journal of Zoology
Italian Journal of Zoology 生物-动物学
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