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. 2020 Jun 8;11:224. doi: 10.1186/s13287-020-01737-0

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Hypoxia-mediated apoptosis is associated with changes in PI3K and AKT. a Co-localization of miR-210 with exosome-specific surface marker CD81 and CD63 by the immunofluorescence. b The uptake of exosome by cardiomyocytes, and the localization of miR-210 molecule with Cy3 fluorescence in cardiomyocytes. c Dual-luciferase reporter assay showed that AIFM3 was a target of miR-210. F, Firefly luciferase; R, Renilla luciferase. d, e AIFM3, p-AKT/AKT, p-PI3K/PI3K, and p-p53/p53 levels were evaluated by Western blotting in cardiomyocytes from the indicated treatment groups ± hypoxia. Quantifications are shown in the lower panel. N = 3 independent experiments. **p < 0.01, ****p < 0.0001 for hypo vs. con. ^##p < 0.01 for hypo + exo vs. hypo