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.
引用
收藏
页数:8
相关论文
共 27 条
[11]   LncRNA-mediated SIRT1/FoxO3a and SIRT1/p53 signaling pathways regulate type II alveolar epithelial cell senescence in patients with chronic obstructive pulmonary disease [J].
Gu, Chao ;
Li, Yaqing ;
Liu, Jialiang ;
Ying, Xiwang ;
Liu, Yuanshun ;
Yan, Jianping ;
Chen, Chun ;
Zhou, Hongbin ;
Cao, Liming ;
Ma, Yingyu .
MOLECULAR MEDICINE REPORTS, 2017, 15 (05) :3129-3134
[12]   Chronic obstructive pulmonary disease (COPD): Neutrophils, macrophages and lymphocytes in patients with anterior tuberculosis compared to tobacco related COPD [J].
Guiedem E. ;
Ikomey G.M. ;
Nkenfou C. ;
Walter P.-Y.E. ;
Mesembe M. ;
Chegou N.N. ;
Jacobs G.B. ;
Okomo Assoumou M.C. .
BMC Research Notes, 11 (1)
[13]  
Hiemstra Pieter S, 2013, Ann Am Thorac Soc, V10 Suppl, pS180, DOI 10.1513/AnnalsATS.201305-123AW
[14]  
Li XF, 2018, 2018 2ND IEEE CONFERENCE ON ENERGY INTERNET AND ENERGY SYSTEM INTEGRATION (EI2), P5
[15]   Chronic obstructive pulmonary disease [J].
Rabe, Klaus F. ;
Watz, Henrik .
LANCET, 2017, 389 (10082) :1931-1940
[16]  
Riedhammer C, 2016, METHODS MOL BIOL, V1304, P53, DOI 10.1007/7651_2014_99
[17]   Pulmonary rehabilitation and COPD: is nonlinear exercise better? [J].
Sant'Anna, Thais ;
Hernandes, Nidia A. ;
Pitta, Fabio .
EXPERT REVIEW OF RESPIRATORY MEDICINE, 2013, 7 (04) :323-325
[18]   NF-kappaB Signaling in Chronic Inflammatory Airway Disease [J].
Schuliga, Michael .
BIOMOLECULES, 2015, 5 (03) :1266-1283
[19]  
Sferrazza Papa G F, 2015, Minerva Med, V106, P9
[20]   Pulmonary Rehabilitation and Physical Activity in Patients with Chronic Obstructive Pulmonary Disease [J].
Spruit, Martijn A. ;
Pitta, Fabio ;
McAuley, Edward ;
ZuWallack, Richard L. ;
Nici, Linda .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2015, 192 (08) :924-933