MiR-21 attenuates apoptosis-triggered by amyloid-ß via modulating PDCD4/ PI3K/AKT/GSK-3ß pathway in SH-SY5Y cells.
Biomed Pharmacother
; 101: 1003-1007, 2018 May.
Article
em En
| MEDLINE
| ID: mdl-29635890
ABSTRACT
Alzheimer's disease (AD) remains the most common neurodegenerative disease with amyloid beta (Aß) formatted and accumulated. Recently, microRNAs have been identified as significant regulators in neurogenesis of the central nervous system (CNS). However, the biological role of miR-21 in AD remains unclear. The purpose of our study was to investigate the mechanism of miR-21 in AD. AD model was established using 20⯵M Aß1-42 in SH-SY5Y cells. Aß1-42 can induce cell apoptosis via increasing Bax and decreasing Bcl-2 protein levels. Meanwhile, we observed that miR-21 was remarkably elevated by indicated Aß1-42 in vitro. Subsequently, miR-21 mimics were transfected into SH-SY5Y cells and it was found that miR-21 can inhibit cell apoptosis induced by Aß1-42. Programmed cell death protein 4 (PDCD4), an important tumor suppressor in various cancers has been reported to prevent AKT activation. The phosphatidylinositol 3-kinase (PI3K)/AKT/GSK-3ß pathway can release a survival signal to protect from multiple injuries. Interestingly, it was found that PDCD4 was involved in miR-21-repressed cell apoptosis in AD models. miR-21 mimics can increase the PI3K, AKT and GSK-3ß activity while PDCD4 ovexexpression inhibited their activity respectively. Moreover, knockdown of PDCD4 can rescue PI3K/AKT/GSK-3ß pathway in SH-SY5Y cells. Taken these together, it was suggested by our data that miR-21 can exert protective roles in AD, which might be dependent on PDCD4/PI3K/AKT/GSK-3ß signaling pathway in vitro.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Transdução de Sinais
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Peptídeos beta-Amiloides
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Proteínas de Ligação a RNA
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Apoptose
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MicroRNAs
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Proteínas Proto-Oncogênicas c-akt
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Proteínas Reguladoras de Apoptose
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Fosfatidilinositol 3-Quinase
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Glicogênio Sintase Quinase 3 beta
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article