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. 2020 Aug 3;10:13016. doi: 10.1038/s41598-020-69495-w

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© The Author(s) 2020

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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Mouse cMSCs’ secretome blocks human ventricular myocyte apoptosis and the dissipation of mitochondrial potential induced by menadione. (a) Representative images and bar graph of TUNEL⁺ vCor.4U human ventricular myocytes, 24 h after menadione ± cMSC-conditioned media at the concentrations shown. n = 9. (b) Representative images and bar graph of mitochondrial TMRM in vCor.4U hPSC-CMs, stressed with menadione ± cMSC-conditioned media. Carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP), oligomycin (Oli) and rotenone (Rot), uncouplers of oxidative phosphorylation, were used as controls. n = 7. (c) Representative images and bar graph of CellROX in vCor.4U hPSC-CMs 8 h after menadione ± cMSC-conditioned media. n = 12. (d) Representative images and bar graph of MitoSOX 4 h after menadione ± cMSC-conditioned media. n = 7. For all panels: scale bar 50 μm; data are shown as the mean ± SEM; *p < 0.05; ***p < 0.0001.