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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
MicroRNA-125b Prevents Cardiac Dysfunction in Polymicrobial Sepsis by Targeting TRAF6-Mediated Nuclear Factor κB
He Ma1,2, Xiaohui Wang1, Tuanzhu Ha1,3
1Department of Surgery.
Background:
This study examined the effect of microRNA-125b (miR-125b) on sepsis-induced cardiac dysfunction.
Methods:
Mouse hearts were transfected with lentivirus expressing miR-125b (LmiR-125b) 7 days before cecal ligation and puncture (CLP)-induced sepsis. Cardiac function was examined by echocardiography before and 6 hours after CLP (n = 6/group). Survival was monitored following CLP-induced sepsis (n = 12/group).
Results:
LmiR-125b transfection significantly attenuated cardiac dysfunction due to CLP-induced sepsis. Fractional shortening and ejection fraction values were significantly (P < .05) higher in the LmiR-125b-treated CLP group than in the untreated CLP group. Survival outcome in LmiR-125b-transfected septic mice was markedly improved, compared with mice with CLP-induced sepsis. Transfection of LmiR-125b into the heart significantly suppressed the expression of ICAM-1 and VCAM-1, decreased the accumulation of macrophages and neutrophils in the myocardium, and decreased serum levels of tumor necrosis factor α and interleukin 1β by targeting tumor necrosis factor receptor-associated factor 6 (TRAF6)-mediated nuclear factor κB (NF-κB) activation. In addition, sepsis-induced myocardial apoptosis was markedly attenuated by LmiR-125b transfection through suppression of p53, Bax, and Bak1 expression. In vitro transfection of endothelial cells with miR-125b mimics attenuate LPS-induced ICAM-1 and VCAM-1 expression by suppressing TRAF6 and NF-κB activation.
Conclusions:
Increased myocardial miR-125b expression attenuates sepsis-induced cardiac dysfunction and improves survival. miR-125b may be a target for septic cardiomyopathy.
Insights
Increased microRNA-125b (miR-125b) expression in the heart protects against sepsis-induced cardiac dysfunction and improves survival. This suggests miR-125b is a potential therapeutic target for septic cardiomyopathy.
Area of Science:
- Cardiology
- Molecular Biology
- Sepsis Research
Background:
- Sepsis frequently leads to cardiac dysfunction, a major cause of mortality.
- MicroRNAs (miRNAs) play critical roles in regulating cardiac function.
- The specific role of microRNA-125b (miR-125b) in sepsis-induced cardiomyopathy requires further investigation.
Purpose of the Study:
- To investigate the therapeutic effect of increased myocardial miR-125b expression on sepsis-induced cardiac dysfunction.
- To elucidate the molecular mechanisms underlying miR-125b's protective effects in sepsis.
Main Methods:
- Mice hearts were transfected with lentivirus expressing miR-125b (LmiR-125b) prior to inducing sepsis via cecal ligation and puncture (CLP).
- Cardiac function was assessed using echocardiography.
- Survival rates and myocardial inflammatory markers were evaluated.
Main Results:
- LmiR-125b transfection significantly attenuated sepsis-induced cardiac dysfunction, improving fractional shortening and ejection fraction.
- Survival rates were markedly improved in LmiR-125b-treated septic mice.
- miR-125b suppressed ICAM-1 and VCAM-1 expression, reduced inflammatory cell infiltration, and decreased pro-inflammatory cytokines by inhibiting TRAF6-mediated NF-κB activation.
- Myocardial apoptosis was reduced by downregulating p53, Bax, and Bak1 expression.
Conclusions:
- Elevated myocardial miR-125b expression confers protection against sepsis-induced cardiac dysfunction and enhances survival.
- miR-125b emerges as a promising therapeutic target for managing septic cardiomyopathy.
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