LncRNA MIR155HG regulates M1/M2 macrophage polarization in chronic obstructive pulmonary disease

被引:72
作者
Li, Nannan [1 ]
Liu, Yuan [2 ]
Cai, Jingfen [1 ]
机构
[1] Nanjing Med Univ, Affiliated Wuxi Matern & Child Hlth Care Hosp, Dept Common Hlth, 48 Huaishu Lane, Wuxi 214002, Jiangsu, Peoples R China
[2] Shanghai Seventh People Hosp, Dept Rehabil, 358 Datong Rd, Shanghai 200137, Peoples R China
关键词
Chronic obstructive pulmonary disease; Macrophage polarization; MIR155HG; LONG NONCODING RNAS; COPD; REHABILITATION; INFLAMMATION; GENE;
D O I
10.1016/j.biopha.2019.109015
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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 macro-phage 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.
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页数:8
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