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. 2020 Jun 29;11:260. doi: 10.1186/s13287-020-01761-0

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© The Author(s) 2020

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

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Fig. 4 — miR-132-3p priming enhanced the effects of MSC-EXs on decreasing ROS production and apoptosis of H/R-injured ECs via activating the PI3K/Akt/eNOS pathway. a–c Representative bands and summarized data showing the protein level of p-Akt/Akt and p-eNOS/eNOS in ECs. d, f Representative images and summarized data showing the ROS production of ECs treated by various MSC-EXs and PI3K inhibitor (LY294002), scale bar = 100 μm. e, g Representative images and summarized data showing the apoptosis of ECs treated by various MSC-EXs and PI3K inhibitor (LY294002). *p < 0.05; n = 3/group