MiR-124-3p attenuates hyperphosphorylation of Tau protein-induced apoptosis via caveolin-1-PI3K/Akt/GSK3ß pathway in N2a/APP695swe cells.
Oncotarget
; 8(15): 24314-24326, 2017 Apr 11.
Article
em En
| MEDLINE
| ID: mdl-28186985
ABSTRACT
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-3ß-Ser9)/GSK-3ß 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/GSK3ß 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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Base de dados:
MEDLINE
Assunto principal:
Proteínas tau
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Fosfatidilinositol 3-Quinases
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MicroRNAs
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Caveolina 1
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Glicogênio Sintase Quinase 3 beta
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article