Journal
NEUROTOXICITY RESEARCH
Volume 38, Issue 2, Pages 524-535Publisher
SPRINGER
DOI: 10.1007/s12640-020-00217-w
Keywords
MiR-539-5p; Amyloid beta-protein production; Tau; Hyperphosphorylation; PI3K/Akt/GSK-3 beta pathway; Alzheimer's disease
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Funding
- Shenzhen Science & Technology Commission [JCYJ20180507184656626]
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The production of amyloid beta (A beta) and tau hyperphosphorylation have been identified as key processes in Alzheimer's disease (AD) pathogenesis. MiR-539-5p has been found to be abnormally expressed in brain tissue; however, the functional role of miR-539-5p in the pathogenesis of AD remains unclear. In our study, we found that the expression of miR-539-5p was significantly downregulated in humans and mice with AD and was negatively correlated with expression of APP, caveolin 1, and GSK-3 beta. Moreover, upregulation of miR-539-5p inhibited A beta accumulation, tau phosphorylation, oxidative stress, and apoptosis and improved memory ability in AD mice. Furthermore, by using bioinformatics tool and dual-luciferase reporter assay, APP, Caveolin 1, and GSK-3 beta were confirmed as direct targets of miR-539-5p. In addition, the PI3K/AKT/GSK-3 beta signaling pathway can be regulated by miR-539-5p. In conclusion, this study provided a novel insight into the pathologic mechanism of AD by identifying that miR-539-5p plays a neuroprotective role in AD.
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