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Updated: Jun 26, 2025
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Deregulated miR-146a-3p alleviates disease progression in atherosclerosis through inactivating NF-κB: An experimental
Taotao Tao1, Linkao Chen, Xia Lin
1Department of Neurology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, Zhejiang, China.
Insights
MicroRNA-146a-3p (miR-146a-3p) inhibits inflammation in atherosclerosis by targeting NF-κB. This miR-146a-3p/NF-κB interaction may offer new biomarkers and therapeutic targets for preventing atherosclerosis and related vascular events.
Area of Science:
- Molecular Biology
- Immunology
- Cardiovascular Research
Background:
- Atherosclerosis (AS) is a complex chronic inflammatory disease and a primary cause of cardiovascular and cerebrovascular diseases.
- Understanding the molecular mechanisms regulating inflammation in AS is crucial for developing effective treatments.
Purpose of the Study:
- To confirm the direct interaction between miR-146a-3p and NF-κB.
- To investigate the role of the miR-146a-3p/NF-κB axis in regulating inflammation during AS progression.
Main Methods:
- Bioinformatic prediction and dual-luciferase reporter assays were employed to validate the miR-146a-3p and NF-κB interaction.
- An in vitro inflammatory cell model of AS was established using lipopolysaccharide stimulation, with pro-inflammatory cytokine levels measured by ELISA.
- Expression levels of miR-146a-3p and NF-κB were quantified using RT-qPCR, and their diagnostic value assessed via ROC curve analysis.
Main Results:
- The AS inflammatory cell model exhibited elevated levels of IL-1β, IL-6, and TNF-α.
- NF-κB was identified as a direct target gene of miR-146a-3p, mediating its inhibitory effects on inflammatory responses.
- In AS patients, the miR-146a-3p/NF-κB pathway correlated with clinical data and inflammatory markers, demonstrating diagnostic accuracy for distinguishing AS from healthy individuals.
Conclusions:
- miR-146a-3p potentially inhibits inflammation in AS by targeting NF-κB.
- The miR-146a-3p/NF-κB pathway presents promising novel biomarkers and therapeutic targets for AS prevention and management of related vascular events.
Background:
Atherosclerosis (AS), as a complex chronic inflammatory disease, is 1 of the main causes of cardiovascular and cerebrovascular diseases. This study aimed to confirm the direct interaction between miR-146a-3p and NF-κB, and explore the role of miR-146a-3p/NF-κB in the regulation of inflammation in AS.
Methods:
Bioinformatic prediction and dual-luciferase reporter assay were used to confirm the interaction between miR-146a-3p and NF-κB. Lipopolysaccharides stimulation was performed to establish AS inflammatory cell model, and the levels of pro-inflammatory cytokines were estimated using an enzyme-linked immunosorbent assay. miR-146a-3p and NF-κB expression were evaluated using reverse transcription quantitative PCR, and their clinical value was examined using a receiver operating characteristic curve.
Results:
Inflammatory cell model showed increased IL-1β, IL-6, and TNF-α. NF-κB was a target gene of miR-146a-3p, and mediated the inhibitory effects of miR-146a-3p on inflammatory responses in the cell model. In patients with AS, miR-146a-3p/NF-κB was associated with patients' clinical data and inflammatory cytokine levels, and aberrant miR-146a-3p and NF-κB showed diagnostic accuracy to distinguish AS patients from healthy populations.
Conclusion:
miR-146a-3p might inhibit inflammation by targeting NF-κB in AS progression, and miR-146a-3p/ NF-κB might provide novel biomarkers and therapeutic targets for the prevention of AS and related vascular events.
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