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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

淀粉样β-寡聚体诱导的线粒体DNA修复受损促成人类神经干细胞分化的改变。

卷 16, 期 10, 2019

页: [934 - 949] 页: 16

弟呕挨: 10.2174/1567205016666191023104036

价格: $65

摘要

背景：在阿尔茨海默氏病（AD）中观察到的神经毒性的近端效应子淀粉样β-42低聚物（Aβ42O），除了会引起线粒体DNA（mtDNA）损伤外，还可以诱导线粒体氧化应激并损害线粒体功能。 Aβ42O还调节干细胞的增殖和分化特性。 目的：我们旨在研究Aβ42O诱导的mtDNA损伤是否参与干细胞分化的调控。 方法：采用人iPSCs衍生的神经干细胞（NSC），分别通过mitoSOX染色和长距离PCR损伤试验研究Aβ42O对活性氧（ROS）产生和DNA损伤的影响。使用线粒体分离物，通过非同源末端连接（NHEJ）体外测定法测定mtDNA修复活性，并通过Western印迹和免疫荧光测定法测定NHEJ成分的表达和定位。分别通过免疫荧光和qPCR检测Tuj-1和GFAP的表达，作为神经元和星形胶质细胞产生的指标。 结果：我们显示，在NSC中，Aβ42O处理可诱导ROS生成和mtDNA损伤，并削弱DNA末端连接活性。 NHEJ组件（例如Ku70 / 80，DNA-PKcs和XRCC4）位于线粒体中，XRCC4的沉默显着加剧了Aβ42O对mtDNA完整性的影响。相反，用植酸（IP6）预处理可特异性刺激DNA-PK依赖性末端连接，可抑制Aβ42O诱导的mtDNA损伤和神经元分化改变。 结论：Aβ42O诱导的mtDNA修复损伤可能改变细胞命运，从而将人NSC分化转移到星形细胞谱系。修复刺激抵消了Aβ420O的神经毒性，表明mtDNA修复途径是治疗AD等神经退行性疾病的潜在靶标。

关键词: 淀粉样β蛋白，线粒体，DNA损伤，DNA修复，人神经干细胞，分化。

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