Open AccessMicroRNA‑125b regulates Alzheimer's disease through SphK1 regulation
Author(s) -
Yan Jin,
Qiuyun Tu,
Min Liu
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9156
Subject(s) - oncogene , sphingosine kinase 1 , microrna , apoptosis , cell cycle , sh sy5y , oxidative stress , molecular medicine , microbiology and biotechnology , cancer research , cell growth , biology , downregulation and upregulation , cell , antagomir , sphingosine , in vitro , neuroblastoma , endocrinology , cell culture , sphingosine 1 phosphate , receptor , gene , biochemistry , genetics
The present study aimed to investigate the expression of microRNA (miR)‑125b in patients with Alzheimer's disease (AD) and to determine its potential role in AD. Mouse neuroblastoma Neuro2a APPSwe/Δ9 cells were used to generate an in vitro AD model. The results demonstrated that the expression levels of miR‑125b were markedly increased in patients with AD compared with in the normal group. In addition, overexpression of miR‑125b significantly inhibited cell proliferation, induced apoptosis, and enhanced inflammation and oxidative stress in an in vitro model of AD model. Furthermore, overexpression of miR‑125b significantly promoted amyloid precursor protein and β‑secretase 1 expression and β‑amyloid peptide production, and suppressed sphingosine kinase 1 (SphK1) protein expression in vitro. These findings suggested that miR‑125b may regulate AD, and neuronal cell growth and apoptosis, via the regulation of inflammatory factors and oxidative stress by SphK1; therefore, miR‑125b may be involved in the development of AD.