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. 2020 May 26;11:200. doi: 10.1186/s13287-020-01733-4

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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. 7 — ADSCs promoted the survival and angiogenesis of parathyroid grafts via inducing FGF2 and VEGF-A through EYA1. a The parathyroid glands were removed from rats and transplanted into nude mice. b The body weights of mice were comparable. c The serum levels of PTH were measured with rat PTH ELISA kit. ADSCs induced PTH levels, and EYA1 inhibitor and VEGF-A antibody abolished this induction, n ≥ 4. d Representative immunochemistry staining of CD31, FGF2, and VEGF-A in parathyroid grafts. e Quantification of vessel numbers per area, as well as FGF2 (surface) and VEGF-a (cytoplasm) levels, n ≥ 3, *p < 0.05