| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-127 |
Sentence |
denotes |
microRNA-218-5p plays a protective role in eosinophilic airway inflammation via targeting δ-catenin, a novel catenin in asthma. |
| T1 |
0-127 |
Sentence |
denotes |
microRNA-218-5p plays a protective role in eosinophilic airway inflammation via targeting δ-catenin, a novel catenin in asthma. |
| T2 |
128-221 |
Sentence |
denotes |
BACKGROUND: microRNA (miR)-218-5p is involved in cigarette smoke-induced airway inflammation. |
| T2 |
128-221 |
Sentence |
denotes |
BACKGROUND: microRNA (miR)-218-5p is involved in cigarette smoke-induced airway inflammation. |
| T3 |
222-323 |
Sentence |
denotes |
In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. |
| T3 |
222-323 |
Sentence |
denotes |
In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. |
| T4 |
324-398 |
Sentence |
denotes |
We hypothesize that miR-218-5p plays a role in asthma airway inflammation. |
| T4 |
324-398 |
Sentence |
denotes |
We hypothesize that miR-218-5p plays a role in asthma airway inflammation. |
| T5 |
399-409 |
Sentence |
denotes |
OBJECTIVE: |
| T5 |
399-409 |
Sentence |
denotes |
OBJECTIVE: |
| T6 |
410-493 |
Sentence |
denotes |
To unveil the role of miR-218-5p and its target gene in asthma airway inflammation. |
| T6 |
410-493 |
Sentence |
denotes |
To unveil the role of miR-218-5p and its target gene in asthma airway inflammation. |
| T7 |
494-502 |
Sentence |
denotes |
METHODS: |
| T7 |
494-502 |
Sentence |
denotes |
METHODS: |
| T8 |
503-703 |
Sentence |
denotes |
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. |
| T8 |
503-703 |
Sentence |
denotes |
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. |
| T9 |
704-900 |
Sentence |
denotes |
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. |
| T9 |
704-900 |
Sentence |
denotes |
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. |
| T10 |
901-1004 |
Sentence |
denotes |
We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation. |
| T10 |
901-1004 |
Sentence |
denotes |
We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation. |
| T11 |
1005-1013 |
Sentence |
denotes |
RESULTS: |
| T11 |
1005-1013 |
Sentence |
denotes |
RESULTS: |
| T12 |
1014-1207 |
Sentence |
denotes |
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. |
| T12 |
1014-1207 |
Sentence |
denotes |
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. |
| T13 |
1208-1280 |
Sentence |
denotes |
We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. |
| T13 |
1208-1280 |
Sentence |
denotes |
We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. |
| T14 |
1281-1480 |
Sentence |
denotes |
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. |
| T14 |
1281-1480 |
Sentence |
denotes |
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. |
| T15 |
1481-1577 |
Sentence |
denotes |
Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. |
| T15 |
1481-1577 |
Sentence |
denotes |
Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. |
| T16 |
1578-1717 |
Sentence |
denotes |
Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. |
| T16 |
1578-1717 |
Sentence |
denotes |
Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. |
| T17 |
1718-1878 |
Sentence |
denotes |
Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. |
| T17 |
1718-1878 |
Sentence |
denotes |
Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. |
| T18 |
1879-2026 |
Sentence |
denotes |
Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model. |
| T18 |
1879-2026 |
Sentence |
denotes |
Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model. |
| T19 |
2027-2062 |
Sentence |
denotes |
CONCLUSIONS AND CLINICAL RELEVANCE: |
| T19 |
2027-2062 |
Sentence |
denotes |
CONCLUSIONS AND CLINICAL RELEVANCE: |
| T20 |
2063-2237 |
Sentence |
denotes |
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. |
| T20 |
2063-2237 |
Sentence |
denotes |
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. |