LncTUG1 Regulates miR-181a/BPIFB4 Axis to Promote COPD Inflammation.

Area of Science:

• Pulmonary Medicine
• Molecular Biology
• Immunology

Background:

• Chronic obstructive pulmonary disease (COPD) involves complex inflammation, high mortality, and morbidity.
• Bactericidal/Permeability-Increasing Fold-Containing Family B member 4 (BPIFB4) is implicated in maintaining inflammatory balance.
• The roles of BPIFB4, miR-181a, and lncRNA TUG1 in COPD inflammation require further elucidation.

Purpose of the Study:

• To investigate the involvement of BPIFB4, miR-181a, and lncRNA TUG1 in the inflammatory processes of COPD.
• To elucidate the regulatory network between these molecules in the context of COPD.
• To explore the potential of targeting these molecules for COPD treatment.

Main Methods:

• Collected induced sputum from COPD patients and healthy controls.
• Utilized THP-1 cells treated with cigarette smoke extract (CSE) for in vitro inflammation modeling.
• Quantified expression levels of BPIFB4, lncTUG1, and miR-181a using qPCR and western blot.
• Employed bioinformatic prediction and dual luciferase assays to determine targeting relationships.
• Assessed macrophage content and inflammatory cytokines via flow cytometry and ELISA.

Main Results:

• BPIFB4 and lncTUG1 expression were elevated in COPD patients, while miR-181a was downregulated.
• BPIFB4 and lncTUG1 were identified as direct targets of miR-181a.
• BPIFB4 overexpression increased M2 macrophages and anti-inflammatory cytokines, whereas silencing BPIFB4 increased M1 macrophages and pro-inflammatory cytokines.
• Silencing lncTUG1 increased miR-181a, decreased BPIFB4, and promoted M1 macrophage polarization and inflammation; overexpression of lncTUG1 had opposite effects.

Conclusions:

• Downregulation of lncTUG1 exacerbates COPD inflammation by reducing BPIFB4 expression through miR-181a.
• Overexpression of BPIFB4 promotes M2 macrophage polarization, alleviating COPD inflammation.
• These findings offer theoretical support and identify potential therapeutic targets for COPD management.