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. 2020 Feb 12;10:2494. doi: 10.1038/s41598-020-59225-7

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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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Long-term pre-treatment for 48 h of normoxic HL1 cardiomyocytes with exosomes (100 μg) derived from hCPCs treated with low-dose ticagrelor (Tic 1 μM) prevents rising of hypoxia inducible factor 1-alpha (HIF1-alpha; 110KDa MW) during severe hypoxia (1% O₂), but not exosomes derived from hCPCs treated with high-dose ticagrelor (Tic 10 μM) (B). Representative images of full-length blots/gels of HIF1-alpha and glyceraldehyde 3-phosphate dehydrogenase (GAPDH; 37KDa MW) are showed in panel A. As shown in panels (D), exosomes released from hCPCs treated in the presence of adenosine (ADE, 10 μM) and EHNA (10 μM) do not reduce intracellular HIF1-alpha levels in hypoxic HL1. Representative images of full-length blots/gels of HIF1-alpha and GAPDH are showed in panel (C). Levels of HIF1-alpha are normalized on GAPDH levels and ratios are expressed as arbitrary units (a.u.). All measurements are mean ± SD. *p < 0.05 vs. untreated condition (Vehicle: sterile phosphate buffer solution); ^#p < 0.05 vs. hypoxia; ^†p < 0.05 vs. Exo-Vehicle.