MicroRNA-125b regulates Alzheimer's disease through SphK1 regulation
MicroRNA-125b regulates Alzheimer's disease through SphK1 regulation
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DOI：
10.3892/mmr.2018.9156
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发表时间：
2018-08-01
影响因子：
3.4
通讯作者：
Liu, Min
中科院分区：
文献类型：
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作者：
Jin, Yan;Tu, Qiuyun;Liu, Min
本研究旨在研究阿尔茨海默病 (AD) 患者中 microRNA (miR)-125b 的表达，并确定其在 AD 中的潜在作用。小鼠神经母细胞瘤 Neuro2a APPSwe/9 细胞用于生成体外 AD 模型。结果表明，与正常组相比，AD患者中miR-125b的表达水平显着升高。此外，在 AD 模型的体外模型中，miR-125b 的过表达显着抑制细胞增殖，诱导细胞凋亡，并增强炎症和氧化应激。此外，miR-125b的过表达显着促进淀粉样前体蛋白和β分泌酶1的表达以及β淀粉样肽的产生，并在体外抑制鞘氨醇激酶1（SphK1）蛋白的表达。这些发现表明，miR-125b 可能通过 SphK1 调节炎症因子和氧化应激来调节 AD 以及神经元细胞生长和凋亡。因此，miR-125b可能参与AD的发生发展。
The present study aimed to investigate the expression of microRNA (miR)-125b in patients with Alzheimer's disease (AD) and to determine its potential role in AD. Mouse neuroblastoma Neuro2a APPSwe/9 cells were used to generate an in vitro AD model. The results demonstrated that the expression levels of miR-125b were markedly increased in patients with AD compared with in the normal group. In addition, overexpression of miR-125b significantly inhibited cell proliferation, induced apoptosis, and enhanced inflammation and oxidative stress in an in vitro model of AD model. Furthermore, overexpression of miR-125b significantly promoted amyloid precursor protein and -secretase 1 expression and -amyloid peptide production, and suppressed sphingosine kinase 1 (SphK1) protein expression in vitro. These findings suggested that miR-125b may regulate AD, and neuronal cell growth and apoptosis, via the regulation of inflammatory factors and oxidative stress by SphK1; therefore, miR-125b may be involved in the development of AD.