Amyloid Beta Peptide 1-42 Induces SH-SY5Y Cell Apoptosis via the Promotion of Meg3 Long Noncoding RNA Expression

Abstract

Background/Aim: The mechanisms and processes of amyloid beta (Aβ) 1-42 /Aβ 1-40 degeneration and deposition of neuron damage are still not clear. The long noncoding RNA (lncRNA) is one of the members of the noncoding RNA family. In this study, we aimed to investigate whether Aβ 1-42 inhibited SH-SY5Y cells in vitro through modulating Meg3 lncRNA. Methods: The Alzheimer's disease (AD) senile plaque cell model was generated using synthetic Aβ 1-42 -treated SH-SY5Y cells. MTT assays were used to determine the proliferation of SH-SY5Y cells. Quantitative (q)RT-PCR and Western blot analyses were used to test the expression levels of mRNA and protein. Northern blot analysis was used to confirm Meg3 lncRNA expression. Results: The MTT assays showed that exogenous Aβ 1-42 suppressed SH-SY5Y cells. The qRT-PCR and Western blot analyses revealed that the expression of p53 mRNA and protein was significantly increased in the AD model group, with a marked decrease in MDM2 and Ki-67 expression on day 7. Moreover, the qRT-PCR and Northern blot analyses confirmed that exogenous Aβ 1-42 promoted the expression of Meg3 lncRNA. There was a downregulation of Meg3 lncRNA expression in SH-SY5Y cells by siRNA, which could promote of the ability of MDM2 to degrade p53 protein on the ubiquitin pathway and delay SH-SY5Y apoptosis. Conclusion: Meg3 lncRNA is implicated as an important factor in the formation of mature Aβ peptides.