Related Experiment Video
Updated: Oct 29, 2026
Lung microRNA Profiling Across the Estrous Cycle in Ozone-exposed Mice
Published on: January 7, 2019
Association of Lung Tissue MicroRNA Expression with Quantitative Emphysema in COPD: An Exploratory Transcriptomic
Taeyun Kim1, Hyunji Choi2, Chul-Ho Oak1
1Division of Pulmonology, Department of Internal Medicine, Kosin University Gospel Hospital, Kosin University College of Medicine, Busan, Republic of Korea.
Background:
MicroRNAs (miRNAs) may participate in biological pathways relevant to emphysema, but their associations with quantitative emphysema in human lung tissue remain uncertain.
Methods:
We analyzed lung tissue miRNA expression and clinical phenotypes from 117 patients with COPD/emphysema in GSE201121. After expression filtering, 839 miRNA loci were evaluated for association with percent emphysema (quantitative CT-derived percent low-attenuation area below -950 HU) using linear regression adjusted for age and sex with HC3 heteroskedasticity-robust standard errors. Multiple testing was controlled using the Benjamini-Hochberg false discovery rate (BH-FDR). Significant loci were collapsed to unique mature miRNAs. Secondary analyses examined associations with FEV1 % predicted, FEV1/FVC, and DLCO. Sensitivity analyses excluded influential observations, used log-transformed percent emphysema, and evaluated former smokers with adjustment for pack-years. Experimentally validated miRNA-target interactions were queried using multiMiR, followed by Gene Ontology Biological Process enrichment.
Results:
Fourteen miRNAs were associated with percent emphysema at BH-FDR <0.05. Eight miRNAs showed positive associations with emphysema (miR-144-5p, miR-190a, miR-20b-5p, miR-451a, miR-3912, miR-15a-5p, miR-202-5p, and miR-4497), whereas six showed negative associations (miR-489, miR-181b-5p, miR-378a-5p, miR-3614-5p, miR-197-3p, and miR-877-3p). Associations with lung function were consistent with the emphysema findings across all 14 miRNAs. After phenotype-specific BH-FDR correction, 12 miRNAs were associated with FEV1 % predicted, 12 with FEV1/FVC, and 8 with DLCO. All 14 associations retained their direction and significance across sensitivity analyses. Enrichment analyses of experimentally supported targets identified processes related to miRNA regulation, apoptosis, hypoxia/oxygen responses, cell-cycle regulation, and vasculature development.
Conclusion:
Lung-tissue expression of 14 mature miRNAs was associated with percent emphysema and lung function in COPD, while target-enrichment findings based on experimentally supported interaction databases were exploratory and require independent and functional validation.
