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Published on: May 31, 2018
MiR-212-3p inhibits LPS-induced inflammatory response through targeting HMGB1 in murine macrophages
Weiwei Chen1, Xiaoying Ma1, Peng Zhang1
1State Key Laboratory of Bioreactor Engineering & Shanghai Key Laboratory of New Drug Design, School of pharmacy, East China University of Science and Technology, Shanghai, PR China.
Abstract:
Sepsis is a major cause of mortality in seriously ill patients characterized by a series of severe systemic inflammatory responses due to an infection. Thus, there is a critically need to search more accurate biomarkers and targets for diagnosis and treatment of sepsis. Our study showed that miR-212-3p was up-regulated in LPS-treated macrophage RAW264.7 cells. Overexpression of miR-212-3p in RAW264.7 cells led to suppression of pro-inflammatory cytokines (TNF-α and IL-6) induced by LPS. Bioinformatic predictions and experimental researches both revealed that HMGB1 was a direct target of miR-212-3p. Meanwhile, the results showed that overexpression of miR-212-3p inhibited the cytoplasmic translocation of HMGB1 in LPS-induced RAW264.7 cells. Subsequently, transfection of the pcDNA3.1/HMGB1 plasmid, which produced HMGB1 overexpression, exhibited similar effects as the LPS-induced macrophage inflammatory response and markedly activated the MAPKs including p38, ERK and JNK phosphorylation. Furthermore, we also found that the phosphorylation of p38 MAPK and ERK was downregulated by miR-212-3p mimics upon LPS injection. In conclusion, these results reveal that miR-212-3p directly targets HMGB1 to suppress inflammatory response in LPS-induced RAW264.7 cells. All our findings indicate that miR-212-3p may act as a potential pharmacological target for promising and effective therapeutic intervention in microbial infection in the future.
Insights
MicroRNA-212-3p targets HMGB1 to reduce inflammation in sepsis models. This finding suggests miR-212-3p as a potential therapeutic target for treating sepsis and other infections.
Area of Science:
- Molecular Biology
- Immunology
- Microbiology
Background:
- Sepsis is a life-threatening condition with high mortality, necessitating novel diagnostic and therapeutic targets.
- Identifying accurate biomarkers for sepsis diagnosis and treatment remains a critical challenge in critical care medicine.
Purpose of the Study:
- To investigate the role of microRNA-212-3p (miR-212-3p) in regulating inflammatory responses in sepsis.
- To identify the molecular targets of miR-212-3p involved in sepsis-induced inflammation.
Main Methods:
- Utilized lipopolysaccharide (LPS)-treated RAW264.7 macrophage cell models.
- Employed bioinformatic analysis and experimental validation to identify miR-212-3p targets.
- Assessed the effects of miR-212-3p and High-Mobility Group Box 1 (HMGB1) on inflammatory cytokine production and MAPK signaling pathways.
Main Results:
- miR-212-3p was upregulated in LPS-treated macrophages and suppressed pro-inflammatory cytokines (TNF-α, IL-6).
- HMGB1 was identified as a direct target of miR-212-3p, and miR-212-3p inhibited HMGB1 cytoplasmic translocation.
- Overexpression of HMGB1 promoted inflammation and activated MAPKs (p38, ERK, JNK); miR-212-3p downregulated p38 and ERK phosphorylation.
Conclusions:
- miR-212-3p directly targets HMGB1 to attenuate inflammatory responses in LPS-induced macrophages.
- miR-212-3p demonstrates potential as a therapeutic target for sepsis and microbial infections.
