Aim
This study explores the mechanism of extracellular vesicles (EVs) derived from human umbilical cord mesenchymal stem cells (hucMSCs) affecting angiogenesis in MI via the microRNA (miR)-423-5p/EFNA3 axis. Material and
Conclusions
EVs promote in vivo angiogenesis in MI rats via the miR-423-5p/EFNA3 axis, thus improving cardiac repair.
Material and methods
HucMSC-derived EVs (hucMSC-EVs) were isolated, extracted, and identified. EVs and human umbilical vein endothelial cells (HUVECs) were co-cultured. Migration capacity and angiogenesis ability of HUVECs were measured, and VEGF levels in cell supernatants were tested by ELISA. In-vivo rat MI models were established, and hucMSC-EVs were injected into the MI rat heart-infarcted area. Cardiac function, capillary density, and the degree of myocardial fibrosis were observed.
Methods
HucMSC-derived EVs (hucMSC-EVs) were isolated, extracted, and identified. EVs and human umbilical vein endothelial cells (HUVECs) were co-cultured. Migration capacity and angiogenesis ability of HUVECs were measured, and VEGF levels in cell supernatants were tested by ELISA. In-vivo rat MI models were established, and hucMSC-EVs were injected into the MI rat heart-infarcted area. Cardiac function, capillary density, and the degree of myocardial fibrosis were observed.
Results
HUVEC migration and angiogenesis were promoted by hucMSC-EVs, and more significantly enhanced by hucMSC-EVs containing miR-423-5p. Furthermore, miR-423-5p inhibited EFNA3 expression and EFNA3 overexpression reversed the promoting effects of EVs on HUVEC migration and angiogenesis. miR-423-5p expression was elevated and EFNA3 expression was reduced in myocardial tissues of MI rats after EV treatment. Both EVs and EVs containing miR-423-5p could improve cardiac function, reduce the area of fibrosis, and promote angiogenesis, improving cardiac repair. Conclusions: EVs promote in vivo angiogenesis in MI rats via the miR-423-5p/EFNA3 axis, thus improving cardiac repair.