LAUSR

Our research proposes to explore the function of miR-140 in the development of COPD. A COPD model was established in rats, and bronchial epithelial cells (BECs) were extracted in the present study, followed by transfection with mimic NC+inhibitor NC, miR-144 mimic, and miR-144 inhibitor. Significantly higher apoptotic rate; downregulated Bcl-2; upregulated Bax and caspase-3; promoted production of IL-6, IL-1β, and MCP-1; higher ROS and MDA levels; lower SOD activity; and inactivated Nrf2 signaling were observed in miR-140 mimic-treated BECs, with opposite results observed in miR-140 inhibitor-treated BECs. The binding site between miR-140 and the 3′UTR region of Nrf2 was predicted and verified using the dual-luciferase gene reporter assay. COPD rats were administered with NC (agomir-NC and antagomir-NC), agomir-140, and antagomir-140. Compared to sham, dramatically lower pulmonary function, higher wet/dry value, severe pathological changes in lung tissues, higher release of inflammatory factors, enhanced apoptosis, higher ROS and MDA levels, lower SOD activity, and inactivated Nrf2 signaling were observed in the model and NC groups, which were greatly aggravated by agomir-140 and significantly reversed by antagomir-140. Collectively, our data suggest that miR-140 aggravates COPD by inducing OS in diaphragm cells by targeting Nrf2.