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Updated: Jun 30, 2026
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
miR-23b Negatively Regulates Sepsis-Induced Inflammatory Responses by Targeting ADAM10 in Human THP-1 Monocytes
Wenying Zhang1, Furong Lu1, Yuliu Xie1
1The Intensive Care Unit, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Background:
Previous studies have demonstrated pivotal roles of disintegrin and metalloproteinase 10 (ADAM10) in the pathogenesis of sepsis. MicroRNA- (miR-) 23b has emerged as an anti-inflammatory factor that prevents multiple autoimmune diseases. However, the underlying mechanisms of miR-23b in the regulation of ADAM10 and sepsis remain uncharacterized.
Methods:
The expression levels of ADAM10 and miR-23b were detected by quantitative RT-PCR and western blot analysis. Cytokine production and THP-1 cell apoptosis were measured by enzyme-linked immunosorbent and annexin V apoptosis assays. Bioinformatics analyses and qRT-PCR, western blot, and luciferase reporter assays were performed to identify ADAM10 as the target gene of miR-23b.
Results:
miR-23b expression was downregulated in the peripheral blood mononuclear cells of sepsis patients and LPS-induced THP-1 cells and was negatively correlated with the expression of ADAM10 and inflammatory cytokines. miR-23b regulated ADAM10 expression by directly binding to the 3'-UTR of ADAM10 mRNA. The overexpression of miR-23b alleviated the LPS-stimulated production of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and apoptosis by targeting ADAM10 in THP-1 cells. The inhibitor or knockdown of ADAM10 elicited effects similar to those of miR-23b on THP-1 cells upon LPS stimulation.
Conclusions:
The present study demonstrated that miR-23b negatively regulated LPS-induced inflammatory responses by targeting ADAM10. The molecular regulatory mechanism of miR-23b in ADAM10 expression and sepsis-induced inflammatory consequences may provide potential therapeutic targets for sepsis.
Insights
MicroRNA-23b targets ADAM10 to reduce sepsis-induced inflammation and cell death. This study reveals miR-23b as a potential therapeutic target for sepsis by regulating ADAM10 expression and inflammatory responses.
Area of Science:
- Molecular Biology
- Immunology
- Sepsis Pathogenesis
Background:
- Disintegrin and metalloproteinase 10 (ADAM10) plays a key role in sepsis.
- MicroRNA-23b (miR-23b) is an anti-inflammatory factor with potential in autoimmune diseases.
- The regulatory mechanism of miR-23b on ADAM10 in sepsis is not well understood.
Purpose of the Study:
- To investigate the role of miR-23b in regulating ADAM10 expression.
- To elucidate the underlying mechanisms of miR-23b in sepsis-induced inflammation.
- To identify potential therapeutic targets for sepsis.
Main Methods:
- Quantitative RT-PCR and western blot analysis to measure ADAM10 and miR-23b expression.
- Enzyme-linked immunosorbent and annexin V apoptosis assays for cytokine production and cell apoptosis.
- Bioinformatics, qRT-PCR, western blot, and luciferase reporter assays to confirm ADAM10 as a miR-23b target.
Main Results:
- miR-23b was downregulated in sepsis patients and LPS-induced cells, correlating negatively with ADAM10 and inflammatory cytokines.
- miR-23b directly binds to the 3'-UTR of ADAM10 mRNA, inhibiting its expression.
- Overexpression of miR-23b reduced inflammatory cytokine production and apoptosis in LPS-stimulated THP-1 cells by targeting ADAM10.
Conclusions:
- miR-23b negatively regulates LPS-induced inflammatory responses by targeting ADAM10.
- The miR-23b/ADAM10 pathway offers a potential therapeutic strategy for sepsis.
- Understanding this molecular mechanism provides insights into sepsis treatment.
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