| Home  | About ScienceAsia  | Publication charge  | Advertise with us  | Subscription for printed version  | Contact us  
Editorial Board
Journal Policy
Instructions for Authors
Online submission
Author Login
Reviewer Login
Volume 50 Number 2
Volume 50 Number 1
Volume 49 Number 6
Volume 49 Number 5
Volume 49S Number 1
Volume 49 Number 4
Earlier issues
Volume  Number 

previous article next article

Research articles

ScienceAsia 49 (2023):ID 805-812 |doi: 10.2306/scienceasia1513-1874.2023.083

MiR-26a-5p promotes Alzheimer's disease by regulating CDK5R1

Dujuan Caoa, Jing Shanga, Chongren Renb,*

ABSTRACT:      Abnormal expression of miRNA is closely associated with disease, particularly Alzheimer?s disease (AD). However, the function of miR-26a-5p in AD pathogenesis is not fully understood. Our aim was to investigate the role of miR-26a-5p and its target gene CDK5R1 during the pathogenesis of AD. In this study, SH-SY5Y cells were treated with beta-amyloid (A?) to create AD mimic cells and MiR-26a-5p, apoptotic biomarkers, and CDK5R1 were evaluated by RT-qPCR. Transfection was performed to downregulate or upregulate miR-26a-5p and CDK5R1 and a molecular correlation between CDK5R1 and miR-26a-5p was predicted using a luciferase reporter assay. Apoptotic biomarkers and proteins associated with the Wnt/?-catenin signaling pathway in AD mimic cells were detected by Western blotting and cell viability was examined using MTT. MiR-26a-5p levels were higher in the A?-coped SH-SY5Y cell lines, which showed reduced viability compared to the control. This effect was reversed when miR-26a-5p was knocked down. MiR-26a-5p has a binding site for CDK5R1, and overexpression of CDK5R1 enhanced cell viability and increased Bcl-2 expression. Furthermore, CDK5R1 overexpression and miR-26a-5p downregulation positively regulated the Wnt/?-catenin signaling pathway. The results showed that MiR-26a-5p is a critical pathogenic gene in AD and its downregulation can be utilized as a novel therapeutic strategy for AD.

Download PDF

135 Downloads 552 Views

a Department of Neurology, Shanxi Bethune Hospital, Taiyuan 030012 China
b Department of General Surgery, Shanxi Bethune Hospital, Taiyuan 030012 China

* Corresponding author, E-mail: renxiangxiang@126.com

Received 11 Feb 2023, Accepted 21 Aug 2023