ArticleJournal of cellular and molecular medicine2020
Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 70 citations in OpenAlex.
- Review
- Clinical significance and mechanistic study of SOX2-OT and miR-27b-3p expression in children with viral myocarditis.BMC pediatrics · 2026Article
- Upregulation of miR-223 by SIRT1 attenuates the inflammatory response in neonatal sepsis.BMC immunology · 2026Article
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- The mechanism of action and therapeutic potential of macrophages in osteoporosis: from polarization balance to targeted regulation.Frontiers in immunology · 2026Review
- Review
- Bioinformatics analysis and experimental validation of potential targets and pathways in chronic kidney disease associated with renal fibrosis.Journal of translational medicine · 2025Article
- Circulating miRNAs are Down-regulated in Asthmatic Patients; Case-control Study.International journal of medical sciences · 2025Article
- Mesenchymal Stem Cell Derived Exosomes Alleviates Hirschsprung-Associated Enterocolitis by Inhibiting AKT Phosphorylation in Macrophages Through miR-223.Stem cells international · 2025Article
- LncRNA MEG3 exacerbates diabetic cardiomyopathy via activating pyroptosis signaling pathway.Frontiers in pharmacology · 2025Article
- The Role of MicroRNA in the Pathophysiology and Diagnosis of Viral Myocarditis.International journal of molecular sciences · 2024Review
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- miR-29b-3p regulates cardiomyocytes pyroptosis in CVB3-induced myocarditis through targeting DNMT3A.Cellular & molecular biology letters · 2024Article
- Long Non-Coding RNAs and Their "Discrete" Contribution to IBD and Johne's Disease-What Stands out in the Current Picture? A Comprehensive Review.International journal of molecular sciences · 2023Review
- Exosomal Non-Coding RNA Mediates Macrophage Polarization: Roles in Cardiovascular Diseases.Biology · 2023Review
- Noncoding RNAs and Cardiac Fibrosis.Reviews in cardiovascular medicine · 2023Review
- Comprehensive overview of microRNA function in rheumatoid arthritis.Bone research · 2023Review
- Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Epigenetic regulation of macrophage polarization in wound healing.Burns & trauma · 2023Review
- The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.Frontiers in genetics · 2023Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral myocarditis (VMC) commonly triggers heart failure, for which no specific treatments are available. This study aims to explore the specific role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) in VMC. A VMC mouse model was induced by Coxsackievirus B3 (CVB3). Then, MEG3 and TNF receptor-associated factor 6 (TRAF6) were silenced and microRNA-223 (miR-223) was over-expressed in the VMC mice, followed by determination of ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Dual-luciferase reporter assay was introduced to test the interaction among MEG3, TRAF6 and miR-223. Macrophages were isolated from cardiac tissues and bone marrow, and polarization of M1 or M2 macrophages was induced. Then, the expressions of components of NLRP3 inflammatory body (NLRP3, ASC, Caspase-1), M1 markers (CD86, iNOS and TNF-α) and M2 markers (CD206, Arginase-1 and Fizz-1) were measured following MEG3 silencing. In the VMC mouse model, MEG3 and TRAF6 levels were obviously increased, while miR-223 expression was significantly reduced. Down-regulation of MEG3 resulted in the inhibition of TRAF6 by promoting miR-223. TRAF6 was negatively correlated with miR-223, but positively correlated with MEG3 expression. Down-regulations of MEG3 or TRAF6 or up-regulation of miR-223 was observed to increase mouse weight, survival rate, LVEF and LVFS, while inhibiting myocarditis and inflammation via the NF-κB pathway inactivation in VMC mice. Down-regulation of MEG3 decreased M1 macrophage polarization and elevated M2 macrophage polarization by up-regulating miR-223. Collectively, down-regulation of MEG3 leads to the inhibition of inflammation and induces M2 macrophage polarization via miR-223/TRAF6/NF-κB axis, thus alleviating VMC.
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