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Fine-tuning the expression of microRNA-155 controls acetaminophen-induced liver inflammation
Kai Yuan1, Xue Zhang2, Lei Lv3
1Department of Vascular Surgery, South Campus, Ren ji Hospital, School of Medicine, Shanghai Jiao Tong University, China.
Abstract:
Treatment of acetaminophen (APAP) in overdose can cause a potentially serious and fatal liver injury. MicroRNA-155 (miR-155), a multifunctional microRNA, is known to mediate inflammatory responses via regulating various target genes. In this study, we aimed to study the role of miR-155 in APAP-induced liver injury, using miR-155-/- mice and miR-155 in vivo intervention. We noted that miR-155 expression was significantly increased in liver and blood after APAP treatment. Knockout of miR-155 deteriorated APAP-induced liver damage, with the elevated serum levels of AST and ALT. The levels of various inflammatory mediators, such as TNF-α and IL-6, were markedly augmented in livers in the absence of miR-155. Moreover, miR-155 deficiency aberrantly activated NF-kappa-B signaling via enhancing p65 and IKKε expression. Finally, in vivo administration of miR-155 agomir attenuated APAP-induced liver damage, reduced the serum levels of AST and ALT, and dampened the NF-kB signaling. In conclusion, our data demonstrated that miR-155 protects the mice against APAP-induced liver damage via mediating NF-KB signaling pathway, suggesting that miR-155 might be a potential pharmaceutic target for treatment of APAP-induced liver inflammation.
Insights
MicroRNA-155 (miR-155) protects against acetaminophen-induced liver injury by regulating inflammatory pathways. Restoring miR-155 levels can mitigate liver damage and inflammation, suggesting its therapeutic potential.
Area of Science:
- Hepatology
- Immunology
- Molecular Biology
Background:
- Acetaminophen (APAP) overdose can lead to severe liver injury.
- MicroRNA-155 (miR-155) plays a role in inflammatory responses.
- The specific role of miR-155 in APAP-induced liver injury requires elucidation.
Purpose of the Study:
- To investigate the role of miR-155 in the pathogenesis of APAP-induced liver injury.
- To explore the potential of miR-155 as a therapeutic target for APAP-induced liver damage.
Main Methods:
- Utilized miR-155 knockout (miR-155-/-) mice and in vivo miR-155 intervention.
- Measured liver injury markers (AST, ALT) and inflammatory mediators (TNF-α, IL-6).
- Assessed NF-kappa-B (NF-kB) signaling pathway activation.
Main Results:
- miR-155 expression increased in liver and blood post-APAP treatment.
- miR-155 deficiency exacerbated APAP-induced liver damage and inflammation.
- miR-155 deficiency led to aberrant NF-kB signaling activation.
- In vivo administration of miR-155 agomir attenuated liver injury and dampened NF-kB signaling.
Conclusions:
- miR-155 exerts a protective effect against APAP-induced liver injury.
- The protective mechanism involves the modulation of the NF-kB signaling pathway.
- miR-155 represents a potential therapeutic target for managing APAP-induced liver inflammation.
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