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. 2021 May 13;9:647763. doi: 10.3389/fcell.2021.647763

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Copyright © 2021 Huang, Chen, Feng, Chen, Yan, Yang, Xiao, Gao, Zhang and Ke.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic illustration/of effect by exosomal mir-1246 and -1290 on myocardial infarction. MiR-1246 and -1290 in EPCs could bind to the promoter of ELF5 and SP1 in HCFs, respectively, and induce their expressions. Resultantly, increased ELF5 and SP1 promoted fibroblast-endothelial transition, demonstrated by increased expressions of endothelial markers, CD31 (by binding to the promoter), VEGFR2, and VE-Cad, and decreased expression of a fibroblast marker, α-SMA. Furthermore, they increased angiogenesis. In rats, both exosomal miR-1246 and -1290 contribute to the exosome-attenuated myocardial infarction (MI). All these indicated that both miR-1246 and -1290 in exosomes from EPCs protected the heart against MI, and this was potentially through increased expressions of ELF5 and SP1.