ArticleTobacco induced diseases2026
MiR-129-5p is associated with chronic obstructive pulmonary disease status and alleviates cigarette smoke extract-induced human bronchial epithelial cell injury.
Article in Tobacco induced diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionChronic obstructive pulmonary disease (COPD) is a common progressive respiratory disease with persistent airflow limitation, chronic airway inflammation, and limited early diagnostic biomarkers and targeted therapies. MicroRNAs (miRNAs) are involved in COPD pathogenesis, but the role of microRNA-129-5p (miR-129-5p) in COPD is unclear. This study investigated miR-129-5p's association with COPD susceptibility, its regulation on cigarette smoke extract (CSE)-induced bronchial epithelial cell injury, and the mechanism involving intercellular cell adhesion molecule 1 (ICAM1) and RELA.
methodsThe study included a cross-sectional study and in vitro experiments. The cross-sectional study (Hanyang Hospital, March 2022-May 2024) collected serum from 126 COPD patients and 120 controls to detect miR-129-5p, ICAM1, and RELA via quantitative real-time polymerase chain reaction (qRT-PCR). Receiver operating characteristic (ROC) curve area (AUC), multivariate logistic regression, and Pearson correlation were used for analysis. In vitro, human bronchial epithelial cells (BEAS-2B) were divided into 6 groups for the CSE-induced injury model; Cell Counting Kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), and dual-luciferase assay detected cell functions and miR-129-5p-ICAM1 targeting.
resultsSerum miR-129-5p was significantly downregulated in COPD patients, with elevated ICAM1, RELA, and inflammatory factors. It distinguished COPD from controls (AUC=0.88; 95% CI: 0.84-0.92, p<0.001) and was an independent susceptibility factor (adjusted odds ratio, AOR=0.15; 95% CI: 0.08-0.26, p<0.001). miR-129-5p was negatively associated with inflammatory factors and positively associated with pulmonary function. CSE inhibited miR-129-5p and induced injury; its overexpression reversed injury, knockdown exacerbated it, and it targeted ICAM1, whose overexpression abrogated miR-129-5p's protection.
conclusionsSerum miR-129-5p was downregulated in COPD patients, while cellular evidence indicated that it potentially alleviates CSE-induced injury by targeting ICAM1 and downregulating RELA, providing preliminary evidence for COPD pathogenesis; further large-scale studies are needed to verify its clinical value.
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