MiR-548ar-3p increases cigarette smoke extractinduced chronic obstructive pulmonary disease (COPD) injury through solute carrier family 17 member 9 (SLC17A9)

Abstract

This study investigated the effect of microRNA mir-548ar-3p on cigarette smoke extract (CSE)-induced chronic obstructive pulmonary disease (COPD). High-throughput sequencing was performed on peripheral blood from smoking COPD patients and non-smoking individuals with normal pulmonary function, and miR-548ar-3p RNA, possessing large differential expression was selected. Experimental groups were divided into control, experimental model (EM), EM+mimic miRNA, negative control (NC) and EM+miR-548ar-3p groups; an empty vector or miR-548ar-3p mimic was transfected into human bronchial epithelial (HBE) cells. A COPD model was established by treating HBE cells with CSE. Cell viability, apoptosis and solute carrier family 17 member 9 (SLC17A9) protein expression were examined by cell counting kit-8, flow cytometry and Western blotting, respectively. Cell viability in the EM+miR-548ar-3p group decreased significantly, and the apoptosis rate and SLC17A9 protein expression increased significantly compared with the control (P<0.05, all groups). In smoking COPD patients, interferon (IFN)-γ and interleukin (IL)-17α expression detected by ELISA was significantly higher than in normal individuals. miR-548ar-3p expression was significantly lower (P<0.05, all groups). These findings suggest that miR-548ar-3p was expressed at a lower level in COPD patients. miR-548ar-3p may increase the extent of CSE-induced COPD injury through SLC17A9.

Keywords

• chronic obstructive pulmonary disease (copd)
• cigarette smoke extract (cse)
• mir-548ar-3p
• solute carrier family 17 member 9 (slc17a9)
• high-throughput sequencing
• human bronchial epithelial cells