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MiR-365-3p is a negative regulator in IL-17-mediated asthmatic inflammation
Weijia Wang1, Ying Li1, Jiaqi Fan1
1The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Background:
Interleukin-17, the major proinflammatory cytokine secreted by Th17 cells, makes essential contribution to pathogenesis of severe asthma, while the detailed mechanisms, especially the involvement of microRNAs which are also important participants in asthma progression, remains largely unclear.
Methods:
In this study, we established a house dust mite (HDM) extract-induced murine asthmatic models and the miRNA expression in the lung tissues of mice were profiled by miRNA microarray assay. The effect of miR-365-3p on IL-17-mediated inflammation was examined by qRT-PCR and immunoblotting analysis. The involvement of ARRB2 as target gene of miR-365-3p was verified by overexpression or RNA interference.
Results:
HDM extract-induced asthmatic inflammation was proved to be IL17-mediated and miR-365-3p was screened out to be the only miRNA exclusively responsive to IL-17. miR-365-3p, whose expression was significantly downregulated upon IL-17 stimulation, was demonstrated to exert remarkable anti-inflammatory effect to decrease IL-17-provoked inflammatory cytokines (KC/IL-8 and IL-6) in both airway epithelial cells and macrophages of murine and human origins, verifying its universal antagonizing activity against IL-17-initiated inflammation across the two species. ARRB2 was characterized as the key target of miR-365-3p to negate IL-17-induced inflammatory cytokines.
Conclusion:
Taken together, our data supported the notion that miR-365-3p, which was diminished by IL-17 in murine and human asthmatic pathogenesis, functioned as an essential negative mediator in IL-17-stimuated inflammatory response by targeting ARRB2, which would shed new light to the understanding and therapeutics thereof of asthmatic inflammation.
Insights
MicroRNA-365-3p acts as a crucial anti-inflammatory agent in asthma by reducing Interleukin-17 (IL-17) driven inflammation. This microRNA targets ARRB2, offering new therapeutic avenues for severe asthma.
Area of Science:
- Immunology
- Molecular Biology
- Respiratory Medicine
Background:
- Severe asthma pathogenesis involves Interleukin-17 (IL-17), a key proinflammatory cytokine.
- The role of microRNAs (miRNAs) in IL-17-mediated asthma mechanisms is not fully understood.
Purpose of the Study:
- To investigate the role of miRNAs in IL-17-driven asthma.
- To identify specific miRNAs that regulate IL-17-mediated inflammation.
- To elucidate the molecular mechanisms underlying miRNA regulation of asthma.
Main Methods:
- Established house dust mite (HDM) extract-induced murine asthma models.
- Profiled miRNA expression in lung tissues using miRNA microarray.
- Assessed miR-365-3p's effect on IL-17-mediated inflammation via qRT-PCR and immunoblotting.
- Verified ARRB2 as a target gene of miR-365-3p using overexpression and RNA interference.
Main Results:
- HDM-induced asthma was confirmed as IL-17-mediated.
- miR-365-3p was identified as the sole miRNA responsive to IL-17 and significantly downregulated by it.
- miR-365-3p demonstrated potent anti-inflammatory effects, reducing IL-17-induced cytokines (KC/IL-8, IL-6) in murine and human airway cells and macrophages.
- ARRB2 was validated as a key target of miR-365-3p in mitigating IL-17-induced inflammation.
Conclusions:
- miR-365-3p acts as a critical negative regulator of IL-17-stimulated inflammation in asthma.
- The miR-365-3p/ARRB2 axis offers novel insights into asthmatic inflammation.
- This pathway presents potential therapeutic targets for severe asthma.
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