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MicroRNA‑125b regulates Alzheimer's disease through SphK1 regulation
Yan Jin1, Qiuyun Tu1, Min Liu1
1Department of Operation Center, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.
Abstract:
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.
Insights
MicroRNA-125b (miR-125b) levels are elevated in Alzheimer's disease (AD). Overexpressing miR-125b worsens AD pathology, suggesting its role in disease development.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and are implicated in various diseases, including AD.
Purpose of the Study:
- To investigate the expression levels of microRNA-125b (miR-125b) in Alzheimer's disease (AD) patients.
- To determine the functional role of miR-125b in AD pathogenesis using an in vitro model.
Main Methods:
- Utilized an in vitro Alzheimer's disease model using mouse neuroblastoma Neuro2a APPSwe/Δ9 cells.
- Quantified miR-125b expression levels.
- Assessed the effects of miR-125b overexpression on cell proliferation, apoptosis, inflammation, oxidative stress, amyloid precursor protein (APP) and β-secretase 1 (BACE1) expression, β-amyloid (Aβ) peptide production, and sphingosine kinase 1 (SphK1) protein expression.
Main Results:
- miR-125b expression was significantly increased in AD patients compared to controls.
- Overexpression of miR-125b inhibited cell proliferation, induced apoptosis, and enhanced inflammation and oxidative stress in the in vitro AD model.
- miR-125b overexpression promoted APP and BACE1 expression, increased Aβ production, and suppressed SphK1 protein levels.
Conclusions:
- miR-125b plays a significant role in Alzheimer's disease pathogenesis.
- miR-125b may regulate neuronal cell growth and apoptosis through the SphK1 pathway, influencing inflammation and oxidative stress.
- miR-125b is a potential therapeutic target for Alzheimer's disease.