LncRNA MIR155HG regulates M1/M2 macrophage polarization in chronic obstructive pulmonary disease - 31/07/19
, Yuan Liu b, 1, Jingfen Cai a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Highlights |
• | MIR155HG is highly expressed in GM-CSF-induced macrophages of COPD patients. |
• | MIR155HG overexpression promotes GM-CSF-induced M1 macrophage polarization and the release of pro-inflammatory cytokines. |
• | Knockdown of MIR-155HG inhibits the polarization of M1 macrophages and increases M2 macrophage polarization. |
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.
Le texte complet de cet article est disponible en PDF.Keywords : Chronic obstructive pulmonary disease, Macrophage polarization, MIR155HG
Plan
Vol 117
Article 109015- septembre 2019 Retour au numéro
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