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. 2021 Feb 3;12:101. doi: 10.1186/s13287-021-02150-x

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© The Author(s) 2021

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. 2 — MiR-205 regulates ECFC angiogenesis in vitro and ex vivo. a–c The results of a Matrigel tube formation assay were assessed 6 h after plating treated ECFCs. d–i Transwell (d–f) and wound healing (g–i) assays confirmed the reduced migration of ECFCs overexpressing miR-205, whereas ECFCs in which miR-205 had been knocked down exhibited enhanced migration. j, k CCK-8 assay results revealed that miR-205 overexpression significantly reduced the viability of ECFCs (j), whereas miR-205 inhibition had the opposite effect (k). l–n CAM assays revealed that miR-205 overexpression significantly decreased vessel density (l), while miR-205 inhibition had the opposite effect (m). Data are means ± S.D (N.S, no significance; ^#P > 0.05, *P < 0.05, **P < 0.01, and ***P < 0.001; n = 3 independent experiments)