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MiR-124-3p helps to protect against acute respiratory distress syndrome by targeting p65
Yufeng Liang1, Junjie Xie2, Di Che3
1Pediatric Intensive Care Unit, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong province, China.
Background:
Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury that has a high mortality rate and leads to substantial healthcare costs. MicroRNA-124-3p (miR-124-3p) helps to suppress inflammation during a pulmonary injury. However, its mechanism of action is largely unknown, and its role in ARDS remains to be determined.
Methods:
Mice and NR8383 cells were exposed to lipopolysaccharides (LPS) to induce ARDS, and their miR-124-3p levels were determined. After a miRNA agomir was administrated to the mice, their pulmonary injuries were evaluated by H&E staining and assays for peripheral inflammatory cytokine levels. The direct interaction between miR-124-3p and p65 was predicted, and then confirmed by a luciferase activity assay. The role played by miRNA-124-3p in regulating p65 expression was further examined by transfection with its agomir, and its role in cell apoptosis was investigated by observing the effects of miRNA overexpression in vitro and in vivo.
Results:
After exposure to LPS, there was a consistent decrease in miR-124-3p expression in the lungs of mice and in NR8383 cells. After treatment with the miR-124-3p agomir, the degrees of pulmonary injury (e.g. alveolar hemorrhage and interstitial edema), and the increases in IL-1β, IL-6, and TNF-α levels induced by LPS were significantly attenuated. Overexpression of miR-124-3p in NC8383 cells and lung tissues significantly suppressed LPS-induced p65 expression and cell apoptosis.
Conclusions:
These results suggest that miR-124-3p directly targeted p65, and thereby decreased the levels of inflammation and pulmonary injury in a mouse model of ARDS.
Insights
MicroRNA-124-3p (miR-124-3p) suppresses inflammation in acute respiratory distress syndrome (ARDS). This study shows miR-124-3p targets p65, reducing lung injury and apoptosis in an ARDS mouse model.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Acute respiratory distress syndrome (ARDS) is a severe lung injury with high mortality.
- MicroRNA-124-3p (miR-124-3p) is known to suppress inflammation but its role in ARDS is unclear.
- The precise mechanism of miR-124-3p in pulmonary injury requires elucidation.
Purpose of the Study:
- To investigate the role and mechanism of miR-124-3p in lipopolysaccharide (LPS)-induced ARDS.
- To determine if miR-124-3p can mitigate lung injury and inflammation in an ARDS model.
- To explore the interaction between miR-124-3p and the p65 signaling pathway.
Main Methods:
- Induced ARDS in mice and NR8383 cells using LPS.
- Administered miR-124-3p agomir to mice and evaluated pulmonary injury and inflammatory cytokines.
- Confirmed the direct interaction between miR-124-3p and p65 using luciferase assays and assessed effects on apoptosis.
Main Results:
- LPS exposure decreased miR-124-3p levels in lung tissues and cells.
- miR-124-3p agomir treatment significantly reduced lung injury and levels of IL-1β, IL-6, and TNF-α.
- Overexpression of miR-124-3p suppressed LPS-induced p65 expression and cell apoptosis in vitro and in vivo.
Conclusions:
- miR-124-3p directly targets p65 in the context of ARDS.
- miR-124-3p exerts protective effects by reducing inflammation and pulmonary injury.
- This finding highlights miR-124-3p as a potential therapeutic target for ARDS.
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