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In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. We hypothesize that miR-218-5p plays a role in asthma airway inflammation.\nOBJECTIVE: To unveil the role of miR-218-5p and its target gene in asthma airway inflammation.\nMETHODS: We measured miR-218-5p expression in bronchial brushings of asthma patients (n = 50) and healthy controls (n = 15), and analysed the correlations between miR-218-5p expression and airway eosinophilia. We examined whether CTNND2 was a target of miR-218-5p, and the expression of 12 catenin family members in bronchial brushings, in cultured human bronchial epithelial (HBE) cells and BEAS-2B cells. We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation.\nRESULTS: Epithelial miR-218-5p expression was significantly decreased and negatively correlated with eosinophils in induced sputum and bronchial biopsies, and other type 2 biomarkers in asthma patients. We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. Remarkably, CTNND2 was the most significantly up-regulated catenin compared with the other 11 catenin family members in bronchial brushings of asthma patients, IL-13-stimulated HBE and BEAS-2B cells. Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model.\nCONCLUSIONS AND CLINICAL RELEVANCE: Epithelial miR-218-5p plays a protective role in eosinophilic airway inflammation via targeting CTNND2, a novel catenin in asthma, and suppressing chemokine CCL26 expression."}

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plays a protective role in eosinophilic airway inflammation via targeting δ-catenin, a novel catenin in asthma.\nBACKGROUND: microRNA (miR)-218-5p is involved in cigarette smoke-induced airway inflammation. In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. We hypothesize that miR-218-5p plays a role in asthma airway inflammation.\nOBJECTIVE: To unveil the role of miR-218-5p and its target gene in asthma airway inflammation.\nMETHODS: We measured miR-218-5p expression in bronchial brushings of asthma patients (n = 50) and healthy controls (n = 15), and analysed the correlations between miR-218-5p expression and airway eosinophilia. We examined whether CTNND2 was a target of miR-218-5p, and the expression of 12 catenin family members in bronchial brushings, in cultured human bronchial epithelial (HBE) cells and BEAS-2B cells. We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation.\nRESULTS: Epithelial miR-218-5p expression was significantly decreased and negatively correlated with eosinophils in induced sputum and bronchial biopsies, and other type 2 biomarkers in asthma patients. We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. Remarkably, CTNND2 was the most significantly up-regulated catenin compared with the other 11 catenin family members in bronchial brushings of asthma patients, IL-13-stimulated HBE and BEAS-2B cells. Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model.\nCONCLUSIONS AND CLINICAL RELEVANCE: Epithelial miR-218-5p plays a protective role in eosinophilic airway inflammation via targeting CTNND2, a novel catenin in asthma, and suppressing chemokine CCL26 expression."}

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":127},"obj":"Sentence"},{"id":"T2","span":{"begin":128,"end":221},"obj":"Sentence"},{"id":"T3","span":{"begin":222,"end":323},"obj":"Sentence"},{"id":"T4","span":{"begin":324,"end":398},"obj":"Sentence"},{"id":"T5","span":{"begin":399,"end":409},"obj":"Sentence"},{"id":"T6","span":{"begin":410,"end":493},"obj":"Sentence"},{"id":"T7","span":{"begin":494,"end":502},"obj":"Sentence"},{"id":"T8","span":{"begin":503,"end":703},"obj":"Sentence"},{"id":"T9","span":{"begin":704,"end":900},"obj":"Sentence"},{"id":"T10","span":{"begin":901,"end":1004},"obj":"Sentence"},{"id":"T11","span":{"begin":1005,"end":1013},"obj":"Sentence"},{"id":"T12","span":{"begin":1014,"end":1207},"obj":"Sentence"},{"id":"T13","span":{"begin":1208,"end":1280},"obj":"Sentence"},{"id":"T14","span":{"begin":1281,"end":1480},"obj":"Sentence"},{"id":"T15","span":{"begin":1481,"end":1577},"obj":"Sentence"},{"id":"T16","span":{"begin":1578,"end":1717},"obj":"Sentence"},{"id":"T17","span":{"begin":1718,"end":1878},"obj":"Sentence"},{"id":"T18","span":{"begin":1879,"end":2026},"obj":"Sentence"},{"id":"T19","span":{"begin":2027,"end":2062},"obj":"Sentence"},{"id":"T20","span":{"begin":2063,"end":2237},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":127},"obj":"Sentence"},{"id":"T2","span":{"begin":128,"end":221},"obj":"Sentence"},{"id":"T3","span":{"begin":222,"end":323},"obj":"Sentence"},{"id":"T4","span":{"begin":324,"end":398},"obj":"Sentence"},{"id":"T5","span":{"begin":399,"end":409},"obj":"Sentence"},{"id":"T6","span":{"begin":410,"end":493},"obj":"Sentence"},{"id":"T7","span":{"begin":494,"end":502},"obj":"Sentence"},{"id":"T8","span":{"begin":503,"end":703},"obj":"Sentence"},{"id":"T9","span":{"begin":704,"end":900},"obj":"Sentence"},{"id":"T10","span":{"begin":901,"end":1004},"obj":"Sentence"},{"id":"T11","span":{"begin":1005,"end":1013},"obj":"Sentence"},{"id":"T12","span":{"begin":1014,"end":1207},"obj":"Sentence"},{"id":"T13","span":{"begin":1208,"end":1280},"obj":"Sentence"},{"id":"T14","span":{"begin":1281,"end":1480},"obj":"Sentence"},{"id":"T15","span":{"begin":1481,"end":1577},"obj":"Sentence"},{"id":"T16","span":{"begin":1578,"end":1717},"obj":"Sentence"},{"id":"T17","span":{"begin":1718,"end":1878},"obj":"Sentence"},{"id":"T18","span":{"begin":1879,"end":2026},"obj":"Sentence"},{"id":"T19","span":{"begin":2027,"end":2062},"obj":"Sentence"},{"id":"T20","span":{"begin":2063,"end":2237},"obj":"Sentence"}],"text":"microRNA-218-5p plays a protective role in eosinophilic airway inflammation via targeting δ-catenin, a novel catenin in asthma.\nBACKGROUND: microRNA (miR)-218-5p is involved in cigarette smoke-induced airway inflammation. In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. We hypothesize that miR-218-5p plays a role in asthma airway inflammation.\nOBJECTIVE: To unveil the role of miR-218-5p and its target gene in asthma airway inflammation.\nMETHODS: We measured miR-218-5p expression in bronchial brushings of asthma patients (n = 50) and healthy controls (n = 15), and analysed the correlations between miR-218-5p expression and airway eosinophilia. We examined whether CTNND2 was a target of miR-218-5p, and the expression of 12 catenin family members in bronchial brushings, in cultured human bronchial epithelial (HBE) cells and BEAS-2B cells. We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation.\nRESULTS: Epithelial miR-218-5p expression was significantly decreased and negatively correlated with eosinophils in induced sputum and bronchial biopsies, and other type 2 biomarkers in asthma patients. We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. Remarkably, CTNND2 was the most significantly up-regulated catenin compared with the other 11 catenin family members in bronchial brushings of asthma patients, IL-13-stimulated HBE and BEAS-2B cells. Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model.\nCONCLUSIONS AND CLINICAL RELEVANCE: Epithelial miR-218-5p plays a protective role in eosinophilic airway inflammation via targeting CTNND2, a novel catenin in asthma, and suppressing chemokine CCL26 expression."}