Mir-129 Promotes the Proliferation of Alzheimer’s Neuronal Cells by Binding the 3′ Untranslated Regions (3′ UTR) of Amyloid Precursor Protein (APP)
Journal of biomaterials and tissue engineering(2022)
摘要
Alzheimer’s disease (AD) is a neurodegenerative disease with memory loss and cognitive impairment. Short non-coding RNAs (miRNAs) are potential biomarkers and therapeutic targets for AD. This study aims to investigate miR-129’s role in AD. miR-129 and amyloid precursor protein (APP) expression was measured by Q-PCR, and LC3, p62, ATG5, Bcl-2, p-Tau and Caspase3 protein was detected by Western blot. Hydrogenase kits and DCFH-DA detected cell apoptosis, cytotoxicity and ROS generation. The interaction between APP and miR-129 was assessed by luciferase report experiment. HE staining and TUNEL assay evaluated hippocampal neuron damage. In AD patient serum, AD transgenic (TG) mouse brain tissue, and AB1-42-treated SH-SY5Y cells, miR-129 was downregulated but autophagy was increased. Overexpression of miR-129 reduced cell damage induced by AB1-42, and miR-129 can directly regulate APP expression by binding APP 3′-UTR. miR-129 inhibitors reversed the protective effect of shAPP on AB1-42-induced cell damage. In addition, miR-129 overexpression reduced neuronal damage through inhibiting autophagy in vivo. APP expression in AD patient and AD cell model was significantly increased compared to controls. Aβ-42 treatment caused up-regulation of APP expression, while APP knockdown inhibited neurons through autophagy. In conclusion, miR-129 overexpression can regulate autophagy by targeting APP5, thereby reducing neuronal damage in AD. These findings provide a new perspective for treating AD.
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关键词
Alzheimer's Disease,MiR-129,Amyloid,Neuron,Autophagy
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