淀粉样前体蛋白
免疫印迹
分子生物学
细胞凋亡
淀粉样蛋白(真菌学)
转染
淀粉样前体蛋白分泌酶
化学
流式细胞术
实时聚合酶链反应
小RNA
阿尔茨海默病
BACE1-AS系列
生物
生物化学
细胞生物学
细胞培养
医学
内科学
疾病
基因
遗传学
无机化学
作者
Xianpei Tan,Yi Luo,Ding-fang Pi,Xia Lie-xin,Zhilian Li,Qiang Tu
出处
期刊:Current Neurovascular Research
[Bentham Science]
日期:2020-01-20
卷期号:17 (1): 86-92
被引量:28
标识
DOI:10.2174/1567202617666200117103931
摘要
Background: Alzheimer’s disease (AD) is the most common neurodegenerative disease, and the accumulation of amyloid-β is the initial process in AD. MicroRNAs (miRNAs) are widely known as key regulators of the accumulation of amyloid-β in AD. This study analyzed the potential effects and possible internal mechanisms of miR-340 on AD. Methods: The expression of miR-340 in senescence-accelerated mouse prone-8 (SAMP8) mouse and senescence-accelerated mice/resistant-1 (SAMR1) mouse was evaluated by qRT-PCR (quantitative real-time polymerase chain reaction). The expression of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) was determined by qRT-PCR and western blot. The binding ability between miR-340 and BACE1 was verified by dual-luciferase reporter assay. In vitro cell model of AD was established in human neuroblastoma SH-SY5Y cells transfected with Swedish mutant form of amyloid precursor protein (APPswe). The effect of miR-340 on the accumulation of amyloid- β was investigated by western blot analysis. Flow cytometry was conducted to detect cell apoptosis. Results: MiR-340 was down-regulated in the hippocampus of AD model SAMP8 mouse compared to SAMR1 mouse, while BACE1 was up-regulated in SAMP8, suggesting a negative correlation between miR-340 and BACE1 in SAMP8 mouse. MiR-340 could directly bind with BACE1, and over-expression of miR-340 decreased expression of BACE1 in SH-SY5Y/APPswe cells. MiR- 340 reduced the accumulation of amyloid-β and suppressed cell apoptosis through targeting BACE1 in SH-SY5Y/APPswe cells. Conclusion: MiR-340 was downregulated in AD and reduced the accumulation of amyloid-β through targeting BACE1, suggesting a potential therapeutic target for AD.
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