ArticleJCI insight2021
Epithelial miR-206 targets CD39/extracellular ATP to upregulate airway IL-25 and TSLP in type 2-high asthma.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Thymic stromal lymphopoietin expression in different biological specimens in asthma: a systematic review and meta-analysis.Frontiers in allergy · 2025Pooled it
- ATP/P2X7 signaling as a potential predictive biomarker for early recurrence of nasal polyps: Correlation with inflammasome activation and epithelial barrier dysfunction.The World Allergy Organization journal · 2026Article
- CPA3 drives the development of asthma by promoting the activation of the JAK/STAT6 pathway.Respiratory research · 2025Article
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- New mechanisms in diisocyanate-mediated allergy/toxicity: are microRNAs in play?Current opinion in allergy and clinical immunology · 2025Review
- Epithelial and immune transcriptomic characteristics and possible regulatory mechanisms in asthma exacerbation: insights from integrated studies.Frontiers in immunology · 2025Article
- Airway epithelial-derived exosomes induce acute asthma exacerbation after respiratory syncytial virus infection.MedComm · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- ATP functions as a primary alarmin in allergen-induced type 2 immunity.American journal of physiology. Cell physiology · 2023Review
- Review
- Phenotype overlap in the natural history of asthma.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- miR-34b/c-5p/CXCL10 Axis Induced by RSV Infection Mediates a Mechanism of Airway Hyperresponsive Diseases.Biology · 2023Article
- Non-Coding RNAs in Pulmonary Diseases: Comparison of Different Airway-Derived Biosamples.International journal of molecular sciences · 2023Review
- Peripheral Multiple Cytokine Profiles Identified CD39 as a Novel Biomarker for Diagnosis and Reflecting Disease Severity in Allergic Rhinitis Patients.Mediators of inflammation · 2023Article
- Recent miRNA Research in Asthma.Current allergy and asthma reports · 2022Review
- Inhibition of Spleen Tyrosine Kinase Restores Glucocorticoid Sensitivity to Improve Steroid-Resistant Asthma.Frontiers in pharmacology · 2022Article
- MicroRNA-182-5p Attenuates Asthmatic Airway Inflammation by Targeting NOX4.Frontiers in immunology · 2022Article
- Exploration of the Molecular Mechanisms ofBioMed research international · 2022Article
- Ruxolitinib Ameliorates Airway Hyperresponsiveness and Lung Inflammation in a Corticosteroid-Resistant Murine Model of Severe Asthma.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial cell-derived cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) initiate type 2 inflammation in allergic diseases, including asthma. However, the signaling pathway regulating these cytokines expression remains elusive. Since microRNAs are pivotal regulators of gene expression, we profiled microRNA expression in bronchial epithelial brushings from type 2-low and type 2-high asthma patients. miR-206 was the most highly expressed epithelial microRNA in type 2-high asthma relative to type 2-low asthma but was downregulated in both subsets compared with healthy controls. CD39, an ectonucleotidase degrading ATP, was a target of miR-206 and upregulated in asthma. Allergen-induced acute extracellular ATP accumulation led to miR-206 downregulation and CD39 upregulation in human bronchial epithelial cells, forming a feedback loop to eliminate excessive ATP. Airway ATP levels were markedly elevated and strongly correlated with IL-25 and TSLP expression in asthma patients. Intriguingly, airway miR-206 antagonism increased Cd39 expression; reduced ATP accumulation; suppressed IL-25, IL-33, and Tslp expression and group 2 innate lymphoid cell expansion; and alleviated type 2 inflammation in a mouse model of allergic airway inflammation. In contrast, airway miR-206 overexpression had opposite effects. Overall, epithelial miR-206 upregulates airway IL-25 and TSLP expression by targeting the CD39-extracellular ATP axis, which represents a potentially novel therapeutic target in type 2-high asthma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.