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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
MiR-342 attenuates lipopolysaccharide-induced acute lung injury via inhibiting MAPK1 expression
Siliang Zhu1, Wenke Song1, Yanqi Sun1
1Department of Intensive Care Unit, Tengzhou Central People's Hospital, Tengzhou, China.
Abstract:
Micro RNA (miRNA) and mitogen-activated protein kinase (MAPK) are reported as the crucial regulators of inflammatory responses in acute lung injury (ALI). This study will explore the role of the miR-342/MAPK1 axis in regulation of lipopolysaccharide (LPS)-induced ALI. We found that miR-342 was down-regulated in LPS-induced A549 cells compared with the control group with DMSO, accompanied by elevated inflammatory cytokines and apoptosis. Over-expression of miR-342 reduced LPS-induced inflammatory responses and apoptosis in LPS-stimulated A549 cells, and had a protective role in LPS-treated mice with ALI by decreasing levels of inflammatory cytokines, improving survival of mice with ALI, and ameliorating the lung permeability. Dual-luciferase reporter gene assay demonstrated that miR-342 regulated the expression of MAPK1 by directly targeting its 3' untranslated region (3'-UTR). Mechanistically, MAPK1 silencing abrogated LPS-induced inflammatory injury in A549 cells, and partially enhanced the protective effect of miR-342. Therefore, miR-342 attenuates LPS-induced ALI by targeting MAPK1 expression, thereby protecting against A549 cell injury induced by LPS and lung injury of mice with ALI.
Insights
MicroRNA-342 (miR-342) protects against acute lung injury (ALI) by targeting MAPK1. Restoring miR-342 levels reduces inflammation and apoptosis in ALI, offering a potential therapeutic strategy.
Area of Science:
- Molecular Biology
- Immunology
- Cell Biology
Background:
- MicroRNAs (miRNAs) and mitogen-activated protein kinases (MAPKs) are key regulators of inflammation in acute lung injury (ALI).
- The specific roles of the miR-342/MAPK1 axis in lipopolysaccharide (LPS)-induced ALI require further elucidation.
Purpose of the Study:
- To investigate the regulatory function of the miR-342/MAPK1 axis in LPS-induced ALI.
- To determine the therapeutic potential of miR-342 in ALI models.
Main Methods:
- Utilized A549 cell lines and a mouse model of LPS-induced ALI.
- Assessed inflammatory cytokine levels, apoptosis, and lung permeability.
- Performed dual-luciferase reporter gene assays to confirm direct targeting of MAPK1 by miR-342.
- Investigated the effects of miR-342 overexpression and MAPK1 silencing.
Main Results:
- miR-342 was significantly downregulated in LPS-induced ALI models, correlating with increased inflammation and apoptosis.
- Overexpression of miR-342 attenuated LPS-induced inflammatory responses and apoptosis in A549 cells and improved survival in ALI mice.
- miR-342 directly targets the 3'-UTR of MAPK1, regulating its expression.
- MAPK1 silencing partially mimicked the protective effects of miR-342 in LPS-induced ALI.
Conclusions:
- miR-342 plays a protective role in LPS-induced ALI by targeting and downregulating MAPK1 expression.
- The miR-342/MAPK1 axis represents a potential therapeutic target for managing acute lung injury.
