Nannan Li1, Yuan Liu2, Jingfen Cai3. 1. Department of Common Health, The Affiliated Wuxi Matemity and Child Health Care Hospital of Nanjing Medical University, No.48 Huaishu Lane, Liangxi District, Wuxi, Jiangsu 214002, China. Electronic address: nannan8098@163.com. 2. Department of Rehabilitation, Shanghai Seventh People' Hospital, No.358 Datong Road, Pudong New District, Shanghai 200137, China. 3. Department of Common Health, The Affiliated Wuxi Matemity and Child Health Care Hospital of Nanjing Medical University, No.48 Huaishu Lane, Liangxi District, Wuxi, Jiangsu 214002, China. Electronic address: ssph1212@sohu.com.
Abstract
BACKGROUND: Macrophages play a crucial role in inflammatory diseases, including chronic obstructive pulmonary disease (COPD). MIR155 host gene (MIR155HG), a novel long non-coding RNA (lncRNA), has been recognized as a regulator of macrophage polarization, we thus investigated its role in COPD. METHODS: We used granulocyte-macrophage colony-stimulating factor (GM-CSF) to induce peripheral blood mononuclear cells (PBMCs)-derived macrophages obtained from COPD patients and normal controls. Quantitative real-time PCR (QRT-PCR) was used to detect the expressions of MIR155HG and M1/M2 macrophage markers. The quantification of M1 and M2 macrophages was analyzed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was conducted for testing the concentration of inflammatory cytokines. RESULTS: MIR155HG was highly expressed in GM-CSF-induced macrophages of COPD patients. Further investigation demonstrated that MIR155HG overexpression promoted GM-CSF-induced M1 macrophage polarization and the release of pro-inflammatory cytokines. However, the knockdown of MIR-155HG could inhibit the polarization of M1 macrophages and increase M2 macrophage polarization. CONCLUSION: LncRNA MIR155HG modulated GM-CSF-mediated M1/M2 macrophage polarization in COPD progression.
BACKGROUND: Macrophages play a crucial role in inflammatory diseases, including chronic obstructive pulmonary disease (COPD). MIR155 host gene (MIR155HG), a novel long non-coding RNA (lncRNA), has been recognized as a regulator of macrophage polarization, we thus investigated its role in COPD. METHODS: We used granulocyte-macrophage colony-stimulating factor (GM-CSF) to induce peripheral blood mononuclear cells (PBMCs)-derived macrophages obtained from COPDpatients and normal controls. Quantitative real-time PCR (QRT-PCR) was used to detect the expressions of MIR155HG and M1/M2 macrophage markers. The quantification of M1 and M2 macrophages was analyzed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was conducted for testing the concentration of inflammatory cytokines. RESULTS:MIR155HG was highly expressed in GM-CSF-induced macrophages of COPDpatients. Further investigation demonstrated that MIR155HG overexpression promoted GM-CSF-induced M1 macrophage polarization and the release of pro-inflammatory cytokines. However, the knockdown of MIR-155HG could inhibit the polarization of M1 macrophages and increase M2 macrophage polarization. CONCLUSION: LncRNA MIR155HG modulated GM-CSF-mediated M1/M2 macrophage polarization in COPD progression.