Circular RNA AXL increases neuron injury and inflammation through targeting microRNA-328 mediated BACE1 in Alzheimer’s disease

基因敲除 炎症 转染 小RNA 神经突 细胞凋亡 癌症研究 下调和上调 细胞生物学 化学 生物 细胞培养 免疫学 基因 体外 生物化学 遗传学
作者
Yuanlong Li,Xiong Han,Hua Fan,Jun Sun,Ming Ni,Lulu Zhang,Fengqin Fang,Wei Zhang,Peizhi Ma
出处
期刊:Neuroscience Letters [Elsevier]
卷期号:776: 136531-136531 被引量:15
标识
DOI:10.1016/j.neulet.2022.136531
摘要

Our previous study observed that circular RNA AXL (circ-AXL, access number circ_0002945) was closely correlated with disease risk and severity of Alzheimer's Disease (AD) by microarray and RT-qPCR validation. Then this current study aimed to further investigate the effect of circ-AXL on regulating neuron injury and inflammation in cellular AD models and its underlying molecular mechanism.SK-N-SH and SK-SY5Y cell lines were treated by amyloid β to construct cellular AD models. Then control or circ-AXL overexpression, control or circ-AXL knock-down, microRNA-328 (miR-328) knock-down with or without circ-AXL knock-down, as well as BACE1 overexpression with or without miR-328 overexpression plasmids were transfected into cellular AD models. Furthermore, neuron injury and inflammation were detected.Circ-AXL overexpression increased apoptosis rate and declined neurite outgrowth, as well as elevated inflammatory cytokines in cellular AD models; but circ-AXL knockdown exhibited opposite effects. Additionally, circ-AXL negatively regulated miR-328 but positively modulated BACE1; besides, miR-328 negatively regulated BACE1; further luciferase reporter gene assay presented that circ-AXL directly bound miR-328, and miR-328 directly bound BACE1. Furthermore, miR-328 overexpression decreased apoptosis rate, elevated neurite outgrowth, and declined inflammatory cytokines in cellular AD models; but miR-328 knockdown presented opposite effects. Notably, miR-328 knockdown attenuated the effect of circ-AXL knockdown on cellular AD models. Moreover, BACE1 overexpression aggravated neuron injury and inflammation, as well as attenuated the effect of miR-328 overexpression on these functions in cellular AD models.Circ-AXL may serve as a potential treatment target via miR-328 mediated BACE1 in AD.
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