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Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
Published on: May 21, 2018
miR-19a-3p inhibition alleviates sepsis-induced lung injury via enhancing USP13 expression
Hangqi Ren1, Wei Mu2, Qiaolian Xu3
1Department of Intensive Care Unit (ICU), The 942 Hospital of PLA, Yinchuan, Ningxia Hui Autonomous Region, 750001, China.
Abstract:
Sepsis is a systemic inflammatory response syndrome caused by various pathogenic microorganisms or toxins. Lung damage is one of the causes of death in patients with sepsis. This study aimed to investigate the role of miR-19a-3p and its regulation mechanism in sepsis-induced lung injury. MH-S cells were treated with lipopolysaccharide (LPS) to establish sepsis-induced lung injury cell model. C57BL/6 mice were injected with miR-19a-3p antagomiR and LPS to construct animal model. LPS-treated and control cells were transfected with miR-19a-3p mimic, miR-19a-3p inhibitor or USP13 expression vector . The expression levels of miR-19a-3p and USP13 were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The concentration of inflammatory cytokines was measured with enzyme-linked immunosorbent assay (ELISA). The relationship of miR-19a-3p and USP13 was validated using dual-luciferase reporter assay. The lung damage was assessed with hematoxylin-eosin staining (HE). The results showed that LPS treatment increased the concentration of TNF-α, IL-6 and IL-1β in MH-S cells. In LPS treated MH-S cells, the level of miR-19a-3p gradually increased over time. Both miR-19a-3p knockdown and USP13 overexpression in MH-S cells inhibited the LPS-induced production of TNF-α, IL-6 and IL-1β. Moreover, miR-19a-3p negatively regulated the expression of USP13 in MH-S cells. Furthermore, miR-19a-3p inhibitor suppressed lung damage in sepsis model mice. In conclusion, miR-19a-3p knockdown could alleviate sepsis-induced lung injury through enhancing USP13 expression.
Insights
Sepsis-induced lung injury involves increased miR-19a-3p. Knocking down miR-19a-3p alleviates lung damage by increasing USP13 expression, offering a potential therapeutic strategy for sepsis.
Area of Science:
- Biomedical Science
- Molecular Biology
- Pathology
Background:
- Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, often leading to organ damage.
- Lung injury is a major cause of mortality in sepsis patients, necessitating research into its underlying mechanisms and potential treatments.
Purpose of the Study:
- To investigate the role of microRNA-19a-3p (miR-19a-3p) in sepsis-induced lung injury.
- To elucidate the regulatory mechanism of miR-19a-3p in the context of lung damage during sepsis.
Main Methods:
- Established cell and mouse models of sepsis-induced lung injury using lipopolysaccharide (LPS).
- Manipulated miR-19a-3p and USP13 expression using mimics, inhibitors, and overexpression vectors.
- Quantified gene and protein expression via qRT-PCR and Western blotting.
- Assessed inflammatory cytokine levels using ELISA and lung tissue damage using HE staining.
Main Results:
- LPS treatment increased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and miR-19a-3p levels in lung cells.
- miR-19a-3p knockdown and USP13 overexpression inhibited LPS-induced inflammation.
- miR-19a-3p was found to negatively regulate USP13 expression.
- Inhibition of miR-19a-3p reduced lung damage in a sepsis mouse model.
Conclusions:
- miR-19a-3p plays a significant role in the pathogenesis of sepsis-induced lung injury.
- Knockdown of miR-19a-3p alleviates lung injury by upregulating USP13 expression.
- Targeting miR-19a-3p presents a potential therapeutic avenue for managing sepsis-induced lung damage.
