Role of miR-211 in a PC12 cell model of Alzheimer's disease via regulation of neurogenin 2

Autor: Da-Peng Zhao, Ai-Ling Yu, Fang-Bo Ning, Wen-Hiu Zhang, Xin-Hong Liu, Hua-Min Wu, Yan-Yan Chang
Rok vydání: 2020
Předmět:
Zdroj: Experimental physiologyREFERENCES. 106(4)
ISSN: 1469-445X
Popis: NEW FINDINGS: What is the central question of this study? The central question of this study is to explore the mechanism of miR-211 on Alzheimer's disease cell model, which is expected to provide a new theoretical basis for the treatment of AD patients. What is the main finding and its importance? miR-211 was upregulated in Alzheimer's disease cell model. miR-211 targeted Ngn2, reduced the activation of PI3K Akt signaling pathway, and inhibited the proliferation of Alzheimer's disease cell model and promoted the apoptosis. ABSTRACT: microRNAs (miRs) are aberrantly expressed in Alzheimer's disease (AD) patients. This study was intended to investigate the effect of miR-211 on AD cell model with the involvement of Neurog 2 (Ngn2). Appropriate dose and time of As1-42 on PC12 cells were determined for AD cell model establishment. Effect of miR-211 expression on cell viability, proliferation and apoptosis was detected after cell transfection. Online prediction and dual luciferase reporter gene assay were utilized to confirm the binding sequence of miR-211 and Ngn2. qRT-PCR and Western blot analysis were applied to measure Ngn2 expression. Gain- and loss- function of miR-211 and Ngn2 was performed, and the activation of the PI3K/Akt signaling pathway was detected. AD cell model was induced by As1-42 treatment. The miR-211 expression was significantly enhanced after miR-211 transfection, leading to suppressed proliferation and promoted apoptosis in As1-42 treated PC12 cells. In addition, miR-211 could downregulate the Ngn2 expression, while overexpression of Ngn2 could reverse the effects of miR-211 on As1-42 -treated PC12 cells and significantly enhance the phosphorylated Akt (P-Akt) and PI3k protein levels. miR-211 could inhibit the growth of PC12 cells via suppressing Ngn2 expression and inactivating the PI3k-Akt signaling pathway. This article is protected by copyright. All rights reserved.
Databáze: OpenAIRE