ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018
Posttranscriptional Regulation of Interleukin-33 Expression by MicroRNA-200 in Bronchial Asthma.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Negative regulation of human IL-33 in endothelium during allergic airway inflammation.JCI insight · 2026Article
- Early-life microRNA signatures in cord blood associated with allergic rhinitis and asthma development.The Journal of allergy and clinical immunology · 2025Article
- Non-Coding RNAs in Pulmonary Diseases: Comparison of Different Airway-Derived Biosamples.International journal of molecular sciences · 2023Review
- Cytokines and microRNAs in SARS-CoV-2: What do we know?Molecular therapy. Nucleic acids · 2022Review
- MicroRNAs-A Promising Tool for Asthma Diagnosis and Severity Assessment: A Systematic Review.Journal of personalized medicine · 2022Review
- Hsa-Mir-320c, Hsa-Mir-200c-3p, and Hsa-Mir-449c-5p as Potential Specific miRNA Biomarkers of COPD: A Pilot Study.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Article
- The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets.Mediators of inflammation · 2022Review
- Review
- Regulation of airway immunity by epithelial miRNAs.Immunological reviews · 2021Review
- Metabolites of intestinal microflora upregulate microRNA-200c-3p expression level to suppress airway epithelial inflammation via the IL6ST/JNK/STAT3 signaling pathway.Experimental and therapeutic medicine · 2021Article
- Plasmid encoding microRNA-200c ameliorates periodontitis and systemic inflammation in obese mice.Molecular therapy. Nucleic acids · 2021Article
- Whole-Transcriptome Sequencing Identifies Key Differentially Expressed mRNAs, miRNAs, lncRNAs, and circRNAs Associated with CHOL.Molecular therapy. Nucleic acids · 2020Article
- MicroRNAs in Asthma and Respiratory Infections: Identifying Common Pathways.Allergy, asthma & immunology research · 2020Review
- Inhibition of miR-378a-3p by Inflammation Enhances IL-33 Levels: A Novel Mechanism of Alarmin Modulation in Ulcerative Colitis.Frontiers in immunology · 2019Article
- Regulatory Mechanisms of IL-33-ST2-Mediated Allergic Inflammation.Frontiers in immunology · 2018Review
- A comprehensive analysis of microRNAs as diagnostic biomarkers for asthma.Therapeutic advances in respiratory diseaseReview
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of understanding how interleukin-33 (IL-33) is regulated (particularly by miRs) is critical in IL-33 biology, and evidence of this in asthma pathology is limited. MicroRNA profiling of cells isolated from bronchoalveolar lavage of 14 asthmatic patients and 11 healthy controls revealed miR-200b and miR-200c were significantly reduced in asthmatic patients compared with healthy controls. The reduction was validated in two independent models of allergen-induced allergic airway inflammation and further demonstrated to be inversely correlated with asthma severity, as well as increased IL-33 production in asthmatic patients. In addition, the miR-200b and miR-200c binding sites in the 3' UTR of IL-33 mRNA were identified by bioinformatics analysis and reporter gene assay. More importantly, introduction of miR-200b and miR-200c reduced, while inhibition of endogenous miR-200b and miR-200c increased, the induction of IL-33 expression in lung epithelial cells. Exogenous administration of miR-200b to lungs of mice with allergic inflammation resulted in a decrease in IL-33 levels and resolution of airway inflammation phenotype. In conclusion, miR-200b and miR-200c by regulating the expression of IL-33 have a role in bronchial asthma, and dysregulation of expression of miR-200b/c may be the underlying mechanism resulting in the asthmatic phenotype.
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