Why the study?
The impact and mechanism of human mesenchymal stem cells on the angiogenesis of cardiac microvascular endothelial cells after ischemia insult were not fully understood.
Does hMSCs-Exo containing miR-543 improve angiogenesis and reduce infarction size in a rat MI model?
Population
Rat myocardial infarction model and isolated rat cardiac microvascular endothelial cells
Comparison
hMSCs-Exo treatment vs exosome inhibitor (GW4869) or miR-543 inhibition
Design
Preclinical in vitro and in vivo animal study
Key result
Human mesenchymal stem cell-derived exosomes facilitated CMEC angiogenesis and reduced infarction size in a rat myocardial infarction model by transferring miR-543 and downregulating COL4A1.
Authors
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Should not yet change MI practice; hypothesis-generating for miR-543 exosome therapy in animal models.
Does hMSCs-Exo containing miR-543 improve angiogenesis and reduce infarction size in a rat MI model?
hMSC-derived exosomes promote angiogenesis and reduce infarct size after myocardial infarction via the miR-543/COL4A1 axis in a rat model.
Yang et al. (2021) studied Myocardial infarction (preclinical model). Human mesenchymal stem cell-derived exosomes (hMSCs-Exo) vs. Control conditions (exosome inhibitor GW4869, miR-543 inhibitor) was evaluated on CMEC proliferation, migration, invasion, angiogenesis, and infarction volume. Human mesenchymal stem cell-derived exosomes facilitated CMEC angiogenesis and reduced infarction size in a rat myocardial infarction model by transferring miR-543 and downregulating COL4A1.