Folia Biologica
Journal of Cellular and Molecular Biology, Charles University 

Chronic obstructive pulmonary disease (COPD) involves persistent airflow limitation and chronic inflammation. To define the clinical and mechanistic role of the miR-532-5p/CXCL1 axis in COPD, this study used bioinformatic analysis of the GEO dataset GSE70080 to identify miR-532-5p, which was significantly down-regulated in COPD. Multiple databases predicted CXCL1 as its potential target gene. The clinical study included 90 subjects (52 with COPD, 38 controls). We detected serum levels of miR-532-5p and CXCL1 mRNA using RT-qPCR and evaluated their diagnostic value through ROC curves and logistic regression. Inflammatory factors (TNF-α, IL-1β) and oxidative stress indicators (SOD, MDA) were measured by ELISA and colorimetry. A dual-luciferase reporter gene assay verified that miR-532-5p directly targets CXCL1. In BEAS-2B cells treated with cigarette smoke extract (CSE), we conducted functional recovery experiments by transfecting miR-532-5p mimics and CXCL1 over-expression vectors to explore their regulatory role in cell injury. The study found that the expression of miR-532-5p in the serum of COPD patients was down-regulated, and its level was correlated with the decline of lung function and the enhancement of inflammation. It also had a diagnostic value for COPD (AUC = 0.8229) and was an independent protective factor. Mechanistically, CXCL1 was confirmed to be a direct target of miR-532-5p; in the cell smoke injury model; miR-532-5p inhibited CXCL1 to alleviate inflammation and oxidative stress. This study identifies miR-532-5p as a potential protective factor in COPD that acts by targeting CXCL1 to mitigate inflammation and oxidative stress, suggesting its diagnostic and therapeutic relevance.

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