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. 2018 Nov 8;8:16519. doi: 10.1038/s41598-018-34879-6

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© The Author(s) 2018

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Cardioprotective effects of cardiomyocyte-exosomes depend on p38/MAPK. (a) Analysis of relative phosphorylation in WT1 and Dys1-iCMs reveals that exosome exposure stimulates phosphorylation of p38 MAPK at 30 minutes. n = 9–12/group, *p < 0.05 vs. 0 min. vehicle, **p < 0.05 Dys-iCM vs. WT-iCM, ^#p = 0.3 vs. vehicle. Blocking p38/MAPK with SB203580 in Dys1-iCMs was associated with (b) increased ROS levels, (c) a decrease in mitochondrial membrane potential, (d) early mPTP formation and (e) increased cell death. n = 3/group. *p < 0.05 vehicle stress vs. vehicle no stress, ^#p < 0.05 exosome exposure vs. vehicle stress, ^&p < 0.05 inhibitor vs. exosome exposure.