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Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
LncRNA MIR155HG regulates M1/M2 macrophage polarization in chronic obstructive pulmonary disease
Nannan Li1, Yuan Liu2, Jingfen Cai1
1Department 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.
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.
Insights
The long non-coding RNA MIR155 host gene (MIR155HG) promotes M1 macrophage polarization in chronic obstructive pulmonary disease (COPD). MIR155HG modulation impacts M1/M2 macrophage balance, suggesting a role in COPD pathogenesis.
Area of Science:
- Immunology
- Molecular Biology
- Respiratory Medicine
Background:
- Macrophages are key players in inflammatory diseases like chronic obstructive pulmonary disease (COPD).
- Long non-coding RNAs (lncRNAs) are emerging as regulators of macrophage function.
- MIR155 host gene (MIR155HG) is a novel lncRNA implicated in macrophage polarization.
Purpose of the Study:
- To investigate the role of MIR155HG in the context of COPD.
- To determine MIR155HG's effect on macrophage polarization in COPD patients.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) from COPD patients and controls were differentiated into macrophages using granulocyte-macrophage colony-stimulating factor (GM-CSF).
- Quantitative real-time PCR (QRT-PCR) and flow cytometry were used to assess MIR155HG expression and M1/M2 macrophage populations.
- Enzyme-linked immunosorbent assay (ELISA) measured inflammatory cytokine levels.
Main Results:
- MIR155HG expression was significantly higher in GM-CSF-induced macrophages from COPD patients.
- Overexpression of MIR155HG enhanced M1 macrophage polarization and pro-inflammatory cytokine release.
- Knockdown of MIR155HG inhibited M1 polarization and promoted M2 macrophage polarization.
Conclusions:
- LncRNA MIR155HG plays a critical role in modulating GM-CSF-mediated M1/M2 macrophage polarization.
- MIR155HG influences COPD progression through its effects on macrophage phenotype.
- Targeting MIR155HG may offer a therapeutic strategy for COPD.
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