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. 2020 Jan 23;11:36. doi: 10.1186/s13287-020-1563-8

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© The Author(s). 2020

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 4 — MiR-144 modulates the effect of MSC-derived exosomes on H9C2 cell apoptosis and p-AKT/AKT expression levels. A The expression of miR-144 was significantly higher in MSC-derived exosomes than in MSCs. ^###P < 0.001 vs. MSCs. B1–B3 Transfection of H9C2 cells with a miR-144 inhibitor partially inhibited the protective effect of MSC-derived exosomes on cell apoptosis in the context of hypoxia. ^###P < 0.001 vs. hypoxia; ^***P < 0.001 vs. hypoxia+Exo. C1–C3 Transfection of H9C2 cells with a miR-144 inhibitor modulated the effect of MSC-derived exosomes on changes in p-AKT/AKT expression levels in hypoxic conditions. ^###P < 0.001 vs. hypoxia; ^***P < 0.001 vs. hypoxia+Exo. MSCs, mesenchymal stem cells; Exo, exosomes; p-AKT/AKT, phosphorylated protein kinase B. Statistics calculated based on the results of three repetitions of each experiment