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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
MicroRNA-762 Modulates Lipopolysaccharide-induced Acute Lung Injury via SIRT7
Cong Wang1, Yun Chen2, Ni-Tao Cheng3
1Department of Hematology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Background:
Inflammation and oxidative stress contribute to the pathogenesis of lipopolysaccharide (LPS)-induced acute lung injury (ALI). MicroRNA-762 (miR-762) has been implicated in the progression of inflammation and oxidative stress; however, its role in ALI remains unclear. In this study, we aim to investigate the role and underlying mechanisms of miR-762 in LPS-induced ALI.
Methods:
Mice were intravenously injected with miR-762 antagomir, agomir or the negative controls for 3 consecutive days and then received a single intratracheal instillation of LPS (5 mg/kg) for 12 h to establish ALI model. Adenoviral vectors were used to knock down the endogenous SIRT7 expression.
Results:
An increased miR-762 expression was detected in LPS-treated lungs. miR-762 antagomir significantly reduced inflammation, oxidative stress and ALI in mice, while the mice with miR-762 agomir treatment exhibited a deleterious phenotype. Besides, we found that SIRT7 upregulation was essential for the pulmonoprotective effects of miR-762 antagomir, and that SIRT7 silence completely abolished the anti-inflammatory and anti-oxidant capacities of miR-762 antagomir.
Conclusion:
miR-762 is implicated in the pathogenesis of LPS-induced ALI via modulating inflammation and oxidative stress, which depends on its regulation of SIRT7 expression. It might be a valuable therapeutic target for the treatment of ALI.
Insights
MicroRNA-762 (miR-762) exacerbates lipopolysaccharide (LPS)-induced acute lung injury (ALI) by increasing inflammation and oxidative stress. Inhibiting miR-762 protects against ALI by upregulating SIRT7, suggesting miR-762 as a therapeutic target.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Inflammation Research
Background:
- Acute lung injury (ALI) pathogenesis involves inflammation and oxidative stress.
- MicroRNA-762 (miR-762) is linked to inflammation and oxidative stress but its role in ALI is unknown.
Purpose of the Study:
- Investigate the role of miR-762 in lipopolysaccharide (LPS)-induced ALI.
- Elucidate the underlying mechanisms of miR-762 action in ALI.
Main Methods:
- Established an LPS-induced ALI mouse model.
- Administered miR-762 antagomir/agomir and used adenoviral vectors for SIRT7 knockdown.
Main Results:
- LPS increased miR-762 expression in lungs.
- miR-762 antagomir reduced inflammation, oxidative stress, and ALI severity.
- miR-762 agomir worsened ALI.
- SIRT7 upregulation was crucial for miR-762 antagomir's protective effects; SIRT7 knockdown abolished these benefits.
Conclusions:
- miR-762 contributes to LPS-induced ALI pathogenesis by modulating inflammation and oxidative stress.
- This effect is dependent on miR-762's regulation of SIRT7 expression.
- miR-762 may represent a therapeutic target for ALI treatment.
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