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Updated: Sep 30, 2025

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Long noncoding RNA MIR3142HG accelerates lipopolysaccharide-induced acute lung injury via miR-95-5p/JAK2 axis
Yanqiu Gao1, Shuangfeng Li2, Rui Dong2
1Respiratory Intensive Care Unit (RICU), Zhengzhou Central Hospital Affiliated to Zhengzhou University, 16 Tongbai North Road, Zhengzhou, 450007, People's Republic of China. hiuk133@163.com.
Abstract:
The study aims to clarify the expression pattern of MIR3142HG in acute lung injury (ALI) and investigate the potential mechanisms for the regulatory role of MIR3142HG in JAK/STAT in ALI. Notably, the ALI patients presented the overexpression of MIR3142HG and JAK2 in their serum samples. Knockdown of MIR3142HG facilitated cell viability but impaired cell apoptosis and inflammatory response via targeting miR-95-5p in lipopolysaccharide (LPS)-treated ALI cells. Overexpression of miR-95-5p promoted cell viability but suppressed apoptosis and inflammatory response via targeting JAK2 in LPS-induced ALI cells. The rescue experiments indicated that inhibition of miR-95-5p could reverse the increased cell viability and promote the inhibited apoptosis and inflammatory response induced by MIR3142HG knockdown in LPS-induced ALI. In conclusion, MIR3142HG is increased in sepsis-induced ALI, and MIR3142HG could accelerate the progression of sepsis-induced ALI through miR-95-5p/JAK2 axis, providing theoretical evidence for MIR3142HG to be a promising target for the therapeutics of ALI.
Insights
MIR3142HG is upregulated in acute lung injury (ALI). This long non-coding RNA accelerates ALI progression by targeting the miR-95-5p/JAK2 pathway, suggesting MIR3142HG as a potential therapeutic target for ALI.
Area of Science:
- Molecular Biology
- Immunology
- Pulmonary Medicine
Background:
- Acute lung injury (ALI) is a critical condition with limited therapeutic options.
- The role of long non-coding RNAs (lncRNAs) like MIR3142HG in ALI pathogenesis is not fully understood.
- The JAK/STAT signaling pathway is implicated in inflammatory responses during ALI.
Purpose of the Study:
- To elucidate the expression profile of MIR3142HG in acute lung injury (ALI).
- To investigate the mechanistic role of MIR3142HG in regulating the JAK/STAT pathway in ALI.
- To explore MIR3142HG as a potential therapeutic target for ALI.
Main Methods:
- Analysis of MIR3142HG and JAK2 expression in serum samples from ALI patients.
- In vitro experiments using lipopolysaccharide (LPS)-induced ALI cell models.
- Knockdown and overexpression of MIR3142HG and miR-95-5p.
- Rescue experiments to validate molecular interactions.
Main Results:
- MIR3142HG and JAK2 were significantly overexpressed in ALI patient serum.
- MIR3142HG knockdown enhanced cell viability and suppressed apoptosis and inflammation in LPS-treated ALI cells via miR-95-5p.
- Overexpression of miR-95-5p promoted cell viability and inhibited apoptosis/inflammation by targeting JAK2 in LPS-induced ALI cells.
- Inhibition of miR-95-5p reversed the effects of MIR3142HG knockdown.
Conclusions:
- MIR3142HG is upregulated in sepsis-induced ALI.
- MIR3142HG exacerbates ALI progression through the miR-95-5p/JAK2 axis.
- MIR3142HG represents a promising therapeutic target for acute lung injury.
Related Concept Videos
The JAK-STAT Signaling Pathway
lncRNA - Long Non-coding RNAs

