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Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
Published on: May 21, 2018
miR-942-5p prevents sepsis-induced acute lung injury via targeting TRIM37
Qiang Lu1, Dinggao Zhang1, Hui Liu1
1Department of Emergency, Yiyang Central Hospital, Yiyang, China.
Abstract:
MicroRNAs (miRNAs) have been demonstrated to play pivotal roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In this work, we aimed to clarify the potential role and the underlying mechanism of miR-942-5p in a lipopolysaccharide (LPS)-induced A549 cell injury model. The cell injury was evaluated by CCK-8 assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-942-5p and tripartite motif-containing protein 37 (TRIM37) were measured by real-time PCR and Western blot, and their association was then validated by bioinformatics, luciferase reporter assay and RNA pull-down assay. We found that the expression of miR-942-5p was decreased in LPS-treated A549 cells. Furthermore, LPS treatment suppressed A549 cell viability, promoted apoptosis and increased the levels of inflammatory cytokines. Conversely, overexpression of miR-942-5p increased cell viability, reduced apoptosis and alleviated inflammatory cytokine secretion in the presence of LPS. Moreover, miR-942-5p directly targeted TRIM37 by binding to the 3'-UTR of TRIM37 mRNA. Upregulation of TRIM37 effectively reversed the anti-apoptotic and anti-inflammatory effects of miR-942-5p in LPS-induced A549 cells. Our findings suggested that miR-942-5p protected against LPS-induced cell injury through inhibiting apoptosis and inflammation in A549 cells by negatively regulating TRIM37.
Insights
MicroRNAs (miRNAs) like miR-942-5p protect lung cells from injury caused by lipopolysaccharide (LPS). This protective effect involves reducing apoptosis and inflammation by targeting TRIM37 expression.
Area of Science:
- Molecular Biology
- Cell Biology
- Immunology
Background:
- MicroRNAs (miRNAs) are key regulators in sepsis-induced acute lung injury (ALI).
- Understanding specific miRNA roles, like miR-942-5p, is crucial for developing therapeutic strategies against ALI.
- Lipopolysaccharide (LPS) is a common trigger for ALI models.
Purpose of the Study:
- To investigate the role and mechanism of miR-942-5p in lipopolysaccharide (LPS)-induced A549 cell injury.
- To determine if miR-942-5p affects apoptosis and inflammation in an ALI model.
- To identify the downstream target of miR-942-5p involved in LPS-induced cell damage.
Main Methods:
- Cell viability assessed by CCK-8 assay, apoptosis by flow cytometry, and inflammatory cytokines by ELISA.
- Expression levels of miR-942-5p and TRIM37 measured using real-time PCR and Western blot.
- miRNA-target interaction validated through bioinformatics, luciferase reporter assays, and RNA pull-down assays.
Main Results:
- LPS treatment decreased miR-942-5p expression in A549 cells, suppressed cell viability, increased apoptosis, and elevated inflammatory cytokine levels.
- Overexpression of miR-942-5p counteracted LPS-induced effects, enhancing cell viability and reducing apoptosis and inflammation.
- miR-942-5p was confirmed to directly target TRIM37, and TRIM37 upregulation reversed the protective effects of miR-942-5p.
Conclusions:
- miR-942-5p plays a protective role against LPS-induced A549 cell injury.
- The mechanism involves miR-942-5p inhibiting apoptosis and inflammation by negatively regulating TRIM37.
- miR-942-5p represents a potential therapeutic target for sepsis-induced acute lung injury.

