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. 2021 May 10;12:281. doi: 10.1186/s13287-021-02349-y

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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. 9 — The proposed molecular mechanism on how TGF-β1 regulate the role of DPSCs in vascular stabilization. TGF-β1 treatment activated Smad2 and Smad3 via phosphorylation, and the activated Smad2 and Smad3 associated with Smad4 regulated Ang1 and VEGF expression besides α-SMA, SM22α. After secretion, Ang1 derived from DPSCs activated its receptor, Tie2, on the HUVEC membrane surface. The activated Ang1/Tie2 promoted VE-Cadherin expression, enhancing cell-cell adhesion and blood vessel stability. The secreted VEGF from DPSCs decreased gradually as DPSCs differentiated into pericyte-like cells, which in turn attenuated VEGF/VEGFR2 signaling, inhibiting HUVEC migration