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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 ERK1/2. (a) Analysis of relative phosphorylation reveals that exosome exposure in WT1 and Dys1-iCMs stimulates phospho-ERK1/2 at 30 minutes. n = 9–12/group, *p < 0.05 vs. 0 min. vehicle, **p < 0.05 Dys-iCM vs. WT-iCM. (b) Trypsinized exosomes failed to stimulate ERK1/2 phosphorylation. Blocking ERK1/2 with U0126 prevented protection leading to (c) increased ROS levels, (d) dissipation of membrane potential, (e) early mPTP formation, and (f) 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.