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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
MIR3142HG promotes lipopolysaccharide-induced acute lung injury by regulating miR-450b-5p/HMGB1 axis
Xiaolei Gong1, Limin Zhu2, Jinlong Liu1,3
1Department of Cardiothoracic Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, No.1678 Dongfang Road, Pudong New Area, Shanghai, 200127, China.
Abstract:
The present study aimed to evaluate the potential roles of MIR3142HG, a novel long non-coding RNA (lncRNA) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was simulated by the treatment of LPS in human pulmonary microvascular endothelial cells (HPMECs). The expression of MIR3142HG, miR-450b-5p and high-mobility group box 1 (HMGB1) was determined by real-time PCR and western blotting. Functional analysis was performed through the assessment of cell viability, apoptosis and the production of proinflammatory cytokines. The interactions among MIR3142HG, miR-450b-5p and HMGB1 were analyzed by bioinformatics methods, dual-luciferase reporter and RNA pull-down assays. Using gain- and loss-of-function approaches, the in vitro functions of MIR3142HG and miR-450b-5p were subsequently assessed. MIR3142HG expression was upregulated, while miR-450b-5p was decreased in LPS-treated HPMECs. MIR3142HG knockdown protected against ALI induced by LPS through alleviating the apoptosis and inflammation of HPMECs. MIR3142HG impaired miR-450b-5p-mediated inhibition of HMGB1. Besides, the effects of MIR3142HG silencing could be alleviated by miR-4262 inhibition or HMGB1 overexpression. MIR3142HG mediated LPS-induced injury of HPMECs by targeting miR-450b-5p/HMGB1, suggesting that MIR3142HG might serve as a therapeutic potential for the treatment of ALI.
Insights
This study reveals MIR3142HG promotes lipopolysaccharide-induced acute lung injury by inhibiting miR-450b-5p and upregulating HMGB1. Silencing MIR3142HG offers a potential therapeutic strategy for acute lung injury.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Acute lung injury (ALI) is a critical condition with limited treatment options.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in disease pathogenesis.
- MIR3142HG is a novel lncRNA whose function in ALI remains largely unexplored.
Purpose of the Study:
- To investigate the role of MIR3142HG in lipopolysaccharide (LPS)-induced ALI.
- To elucidate the molecular mechanism involving MIR3142HG, miR-450b-5p, and high-mobility group box 1 (HMGB1) in ALI.
- To assess the therapeutic potential of targeting MIR3142HG for ALI treatment.
Main Methods:
- Lipopolysaccharide (LPS) was used to induce ALI in human pulmonary microvascular endothelial cells (HPMECs).
- Expression levels of MIR3142HG, miR-450b-5p, and HMGB1 were quantified using real-time PCR and western blotting.
- Functional assays included cell viability, apoptosis, cytokine production, bioinformatics analysis, dual-luciferase reporter assays, and RNA pull-down assays.
Main Results:
- MIR3142HG expression was significantly upregulated, while miR-450b-5p was downregulated in LPS-treated HPMECs.
- Knockdown of MIR3142HG attenuated LPS-induced apoptosis and inflammation in HPMECs.
- MIR3142HG was found to impair the inhibitory effect of miR-450b-5p on HMGB1, suggesting a regulatory axis.
Conclusions:
- MIR3142HG exacerbates LPS-induced ALI by targeting the miR-450b-5p/HMGB1 pathway.
- MIR3142HG knockdown demonstrates protective effects against ALI in vitro.
- MIR3142HG represents a potential therapeutic target for the treatment of acute lung injury.
