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Abstract
Background
Myocardial infarction is the primary cause of high disability and mortality in patients with cardiovascular disease worldwide. The pathological process of myocardial ischemia/reperfusion (I/R) may trigger harmful inflammatory response and ultimately lead to serious cardiac dysfunction. The mechanism of myocardial repair post myocardial infarction has not been fully elucidated. The present study speculated that VSIG4 is related to the regulation of heart injury.
Methods
The myocardial I/R injury model was established in Sprague-Dawley (SD) rats. Before I/R operation, the viral solution containing AAV-NC or AAV-VSIG4 was intravenously injected into rats. Cardiac function indicators, mRNA expression, the apoptosis ratio of cardiomyocytes, myocardial infarct area, phenotype polarization of macrophage, and the protein expression of apoptosis or macrophage phenotype were measured.
Results
Myocardial I/R injury decreased the expression of VSIG4 and subsequently triggered myocardial apoptosis. The induction of AAV-VSIG4 produced a protective effect on general cardiac function and attenuated the I/R-induced cellular apoptosis in rats. Moreover, VSIG4 signaling might potentially modulate macrophage M1/M2-related inflammatory disorders via activation of PI3K/AKT and inhibition of TLR4/NF-κB expression.
Conclusion
In summary, the present study provided evidence that VSIG4 had cardiac protective role in myocardial I/R injury. More importantly, enhanced VSIG4 expression inhibited M1 polarization of macrophages by blocking TLR4/NF-κB activation, subsequently suppressing cardiomyocyte apoptosis. This finding provides vital insights into the role of VSIG4 in I/R injury and may provide a new target for I/R therapy.
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Editor-in-Chief
László ROSIVALL (Semmelweis University, Budapest, Hungary)
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- Ákos KOLLER (Semmelweis University, Budapest, Hungary)
- Zsolt RADÁK (University of Physical Education, Budapest, Hungary)
- László LÉNÁRD (University of Pécs, Hungary)
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- Magdolna DANK (Semmelweis University, Budapest, Hungary)
- László DÉTÁRI (Eötvös Loránd University, Budapest, Hungary)
- Zoltán GIRICZ (Semmelweis University, Budapest, Hungary and Pharmahungary Group, Szeged, Hungary)
- Zoltán HANTOS (Semmelweis University, Budapest and University of Szeged, Hungary)
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- László HUNYADI (Semmelweis University, Budapest, Hungary)
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- Zoltán KARÁDI (University of Pecs, Hungary)
- Miklós PALKOVITS (Semmelweis University, Budapest, Hungary)
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- András SPÄT (Semmelweis University, Budapest, Hungary)
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