Mir-124-3p Attenuates Hyperphosphorylation of Tau Protein-Induced Apoptosis Via Caveolin-1-Pi3k/Akt/Gsk3β Pathway in N2a/App695swe Cells

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  • 作者：Kang, Q., Xiang, Y., Li, D., Liang, J., Zhang, X., Zhou, F., Qiao, M., Nie, Y., He, Y., Cheng, J., Dai, Y. & Li, Y.
  • 期刊：Oncotarget 8, 24314-24326 (2017)
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Hyperphosphorylation of Tau forming neurofibrillary tangles has been considered as a crucial event in the pathogenesis of Alzheimer's disease (AD). MiR-124-3p belongs to microRNA (miRNA) family and was markedly decreased in AD, however, the functions of miR-124-3p in the pathogenesis of AD remain unknown. We observed that the expression of miR-124-3p was significantly decreased in N2a/APP695swe cells; and transfection of miR-124-3p mimics not only attenuated cell apoptosis and abnormal hyperphosphorylation of Tau protein without any changes of total Tau protein, but also increased expression levels of Caveolin-1, phosphoinositide 3-kinase (PI3K), phospho-Akt (Akt-Ser473)/Akt, phospho-glycogen synthase kinase-3 beta (GSK-3β-Ser9)/GSK-3β in N2a/APP695swe cells. We further found that miR-12-3p directly targeted Caveolin-1; miR-124-3p inhibited abnormal hyperphosphorylation of Tau by regulating Caveolin-1-PI3K/Akt/GSK3β pathway in AD. This study reveals that miR-124-3p may play a neuroprotective role in AD, which may provide new ideas and therapeutic targets for AD.

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