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Published on: February 21, 2011
MiR-129-5p is associated with chronic obstructive pulmonary disease status and alleviates cigarette smoke
Dan Liu1, Jingfan Wang2, Ping Zhang2
1Department of Respiratory and Critical Care Medicine, The Fifth Hospital of Wuhan, Wuhan, China.
Introduction:
Chronic 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.
Methods:
The 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.
Results:
Serum 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.
Conclusions:
Serum 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.
Insights
MicroRNA-129-5p (miR-129-5p) is downregulated in chronic obstructive pulmonary disease (COPD) patients. This microRNA (miRNA) may protect against lung injury by targeting ICAM1 and RELA, suggesting a role in COPD pathogenesis.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Biochemistry
Background:
- Chronic obstructive pulmonary disease (COPD) is a progressive respiratory illness characterized by airflow limitation and inflammation.
- Current diagnostic biomarkers and targeted therapies for COPD are limited.
- MicroRNAs (miRNAs) are implicated in COPD pathogenesis, but the specific role of microRNA-129-5p (miR-129-5p) remains unclear.
Purpose of the Study:
- To investigate the association between miR-129-5p and COPD susceptibility.
- To examine the regulatory role of miR-129-5p in cigarette smoke extract (CSE)-induced bronchial epithelial cell injury.
- To elucidate the underlying mechanism involving intercellular cell adhesion molecule 1 (ICAM1) and RELA.
Main Methods:
- A cross-sectional study involving 126 COPD patients and 120 controls, measuring serum miR-129-5p, ICAM1, and RELA using quantitative real-time polymerase chain reaction (qRT-PCR).
- Statistical analyses included receiver operating characteristic (ROC) curve analysis, multivariate logistic regression, and Pearson correlation.
- In vitro experiments utilized human bronchial epithelial cells (BEAS-2B) to model CSE-induced injury, assessing cell viability, apoptosis, inflammatory markers, and the miR-129-5p-ICAM1 interaction via dual-luciferase assays.
Main Results:
- Serum miR-129-5p was significantly downregulated in COPD patients compared to controls (AUC=0.88).
- Lower miR-129-5p levels were independently associated with COPD susceptibility (AOR=0.15) and correlated negatively with inflammatory markers and positively with pulmonary function.
- Overexpression of miR-129-5p mitigated CSE-induced bronchial epithelial cell injury, while its inhibition exacerbated it; miR-129-5p directly targeted ICAM1, and ICAM1 overexpression reversed the protective effects of miR-129-5p.
Conclusions:
- Serum miR-129-5p is downregulated in COPD patients, suggesting its potential as a diagnostic biomarker.
- In vitro findings indicate that miR-129-5p may alleviate CSE-induced lung injury by targeting ICAM1 and downregulating RELA.
- These results provide preliminary evidence for miR-129-5p's role in COPD pathogenesis, warranting further large-scale validation studies for clinical application.
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