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

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