Key result
Human umbilical cord MSC-derived EVs loaded with miR-223 mitigated myocardial infarction and promoted myocardial repair through the P53/S100A9 axis in rat models.
Why the study?
Mesenchymal stem cell-derived extracellular vesicles have been proposed as a promising strategy for MI, but the mechanism of human umbilical cord MSC-derived extracellular vesicles loaded with miR-223 remained to be explored.
Do human umbilical cord MSC-derived EVs loaded with miR-223 ameliorate myocardial infarction in preclinical models?
Do human umbilical cord MSC-derived EVs loaded with miR-223 ameliorate myocardial infarction in preclinical models?
HucMSC-derived EVs loaded with miR-223 show potential for myocardial repair post-MI by targeting the P53/S100A9 axis in preclinical models.
No immediate change to MI management; extends randomized preclinical evidence for engineered EV therapies.
Mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) have been proposed as a promising strategy for myocardial infarction (MI). This study aims to explore the mechanism of human umbilical cord MSCs (hucMSCs)-derived EVs loaded with miR-223 on MI. Inflammation, cell biological functions, and fibrosis in vitro were measured. Furthermore, MI rat models were established to verify the role of EVs-miR-223 in vivo. The binding relationship between miR-223 and P53 was confirmed. ChIP assay was utilized to observe the combination of P53 and S100A9. The suppressed fibrosis of cardiomyocytes occurred with cells overexpressing miR-223. MiR-223 contributed to the angiogenesis of HUVECs. P53 was a target gene of miR-223. In vivo, miR-223 relieved myocardial fibrosis and inflammation infiltration, and promoted the angiogenesis in MI rats. HucMSC-derived EVs loaded with miR-223 mitigates MI and promotes myocardial repair through the P53/S100A9 axis, manifesting the underlying therapy values of hucMSC-derived EVs loaded with miR-223 in MI.
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Yang et al. (2022) studied Myocardial infarction. Human umbilical cord MSCs (hucMSCs)-derived EVs loaded with miR-223 was evaluated on Myocardial fibrosis, inflammation infiltration, and angiogenesis. Human umbilical cord MSC-derived EVs loaded with miR-223 mitigated myocardial infarction and promoted myocardial repair through the P53/S100A9 axis in rat models.
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