Atorvastatin-pretreated mesenchymal stem cell-derived extracellular vesicles significantly improved left ventricular ejection fraction to 52.89% compared to 29.31% with untreated vesicles in a rat model of acute myocardial infarction.
Do atorvastatin-pretreated mesenchymal stem cell-derived extracellular vesicles promote cardiac repair after myocardial infarction?
Atorvastatin-pretreated MSC-derived EVs facilitate cardiac repair in acute myocardial infarction by promoting macrophage polarization via the miR-139-3p/Stat1 pathway.
Absolute Event Rate: 52.89% vs 29.31%
p-value: p=<0.0001
BACKGROUND: -EV. METHODS: -EV and MSC-EV. Macrophages were isolated from rat bone marrow for molecular mechanism analysis. miRNA mimics or inhibitors were transfected into EVs or macrophages to analyze its effects on macrophage polarization and cardiac repair in vitro and in vivo. RESULTS: -EV loaded with miR-139-3p inhibitors decreased while MSC-EV loaded with miR-139-3p mimics increased the expressions of M2 markers and cardioprotective efficacy. CONCLUSIONS: -EV remarkably facilitate cardiac repair in AMI by promoting macrophage polarization via miR-139-3p/Stat1 pathway, which has the great potential for clinical translation.
Ning et al. (Thu,) conducted a other in Acute myocardial infarction (AMI). Atorvastatin-pretreated mesenchymal stem cell-derived extracellular vesicles (MSCATV-EV) vs. MSC-EV (untreated MSC-derived EVs) or PBS was evaluated on Left ventricular ejection fraction (LVEF) on day 28 post-AMI (p=<0.0001). Atorvastatin-pretreated mesenchymal stem cell-derived extracellular vesicles significantly improved left ventricular ejection fraction to 52.89% compared to 29.31% with untreated vesicles in a rat model of acute myocardial infarction.