MiR‑186‑5p regulates the inflammatory response of chronic obstructive pulmonary disorder by targeting HIF‑1α.

Abstract

Chronic obstructive pulmonary disorder (COPD) is a chronic respiratory disease that is a major cause of morbidity and mortality worldwide. Previous studies have shown that miR‑186‑5p expression is significantly increased in COPD and is involved in multiple physiological and pathological processes. However, the role of miRNA‑186‑5p in the inflammatory response of COPD remains unclear. In this study, an invitro model of COPD was established using lipopolysaccharide (LPS)‑induced human bronchial epithelial cells (BEAS‑2B). CCK‑8 assays, flow cytometry, and a Muse cell analyzer were used to determine cell viability, cell cycle distribution, and apoptosis, respectively. The production of TNF‑α and IL‑6 were measured by ELISA. Reverse‑transcription‑quantitative PCR and western blotting were used to analyze mRNA and protein expression levels. The targeting relation between miR‑186‑5p and HIF‑1α was discovered using dual‑luciferase reporter assays. The results showed that transfection of miR‑186‑5p inhibitor inhibited cell proliferation and promoted cell apoptosis in the LPS‑induced BEAS‑2B cells. Inhibition of miR‑186‑5p markedly increased the levels of TNF‑α and IL‑6. miR‑186‑5p directly targeted and negatively regulated HIF‑1α expression. In addition, inhibition of miR‑186‑5p increased the expression of the NF‑κB pathway protein p‑p65. In conclusion, it was found that inhibiting miR‑186‑5p may improve inflammation of COPD through HIF‑1α in LPS‑induced BEAS‑2B cells, possibly by regulating NF‑κB signaling. These findings provide a novel potential avenue for the clinical management of COPD. Future research is required to determine the mechanism of the interaction between miR‑186‑5p and HIF‑1α in COPD.