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LSC Abstract – microRNA profiling reveals a role for microRNA-218-5p in the pathogenesis of chronic obstructive pulmonary disease

Griet Conickx, Pieter Mestdagh, Francisco Avila Cobos, Fien Verhamme, Tania Maes, Bart Vanaudenaerde, Lies Lahousse, Guy Joos, Jo Vandesompele, Ken Bracke, Guy Brusselle
European Respiratory Journal 2016 48: PA4025; DOI: 10.1183/13993003.congress-2016.PA4025
Griet Conickx
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Pieter Mestdagh
2Center for Medical Genetics, Ghent University, Ghent, Belgium
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Francisco Avila Cobos
2Center for Medical Genetics, Ghent University, Ghent, Belgium
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Fien Verhamme
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Tania Maes
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Bart Vanaudenaerde
3Clinical and Experimental Medicine, KULeuven, Leuven, Belgium
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Lies Lahousse
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Guy Joos
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Jo Vandesompele
2Center for Medical Genetics, Ghent University, Ghent, Belgium
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Ken Bracke
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Guy Brusselle
1Respiratory Medicine, Ghent University, Ghent, Belgium
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Abstract

Rationale: Since aberrant expression of microRNAs (miRNAs) has been implicated in disease pathogenesis, we aimed to identify dysregulated miRNAs in lungs of patients with COPD.

Methods: We performed miRNA and mRNA profiling on lung tissue of a screening cohort (n=30) encompassing never smokers, smokers without airflow limitation and smokers with COPD. Differential expression of microRNA-218-5p (miR-218-5p) was validated by RT-qPCR in an independent cohort (n=71). Localization of miR-218-5p was assessed by in situ hybridization. Perturbation of miR-218-5p was obtained by transfecting primary normal human bronchial epithelial (NHBE) cells with a miR-218-5p inhibitor or mimic, followed by polyA-sequencing and RT-qPCR for target genes and markers of inflammation.

Results: Several miRNAs were differentially expressed among the different patient groups. Interestingly, miR-218-5p was significantly down-regulated in smokers without airflow limitation and in patients with COPD, compared to never smokers. Decreased pulmonary expression of miR-218-5p was confirmed in an independent validation cohort. Importantly, expression of miR-218-5p strongly correlated with airflow limitation (FEV1, FEV1/FVC) and lung diffusion (DLCO, KCO). Cellular localization of miR-218-5p revealed highest expression of miR-218-5p in bronchial airway epithelium. Additionally, in vitro perturbation of miR-218-5p in NHBE cells together with gene set enrichment analysis suggest an involvement of miR-218-5p in inflammatory and immune responses.

Conclusions: These translational research findings highlight a potential role for miR-218-5p in the pathogenesis of COPD.

This abstract has been presented previously at the European Respiratory Society's Lung Science Conference in March 2016.

  • Copyright ©the authors 2016
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LSC Abstract – microRNA profiling reveals a role for microRNA-218-5p in the pathogenesis of chronic obstructive pulmonary disease
Griet Conickx, Pieter Mestdagh, Francisco Avila Cobos, Fien Verhamme, Tania Maes, Bart Vanaudenaerde, Lies Lahousse, Guy Joos, Jo Vandesompele, Ken Bracke, Guy Brusselle
European Respiratory Journal Sep 2016, 48 (suppl 60) PA4025; DOI: 10.1183/13993003.congress-2016.PA4025

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LSC Abstract – microRNA profiling reveals a role for microRNA-218-5p in the pathogenesis of chronic obstructive pulmonary disease
Griet Conickx, Pieter Mestdagh, Francisco Avila Cobos, Fien Verhamme, Tania Maes, Bart Vanaudenaerde, Lies Lahousse, Guy Joos, Jo Vandesompele, Ken Bracke, Guy Brusselle
European Respiratory Journal Sep 2016, 48 (suppl 60) PA4025; DOI: 10.1183/13993003.congress-2016.PA4025
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