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. 2017 Jul 6;18:55. doi: 10.1186/s40360-017-0163-4

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 3 — Sema3A inhibits VEGF-induced angiogenesis. a, a endothelial cells cultured with starvation medium from SSC-9; b endothelial cells cultured with starvation medium from SSC-9 with Sema3A overexpression. b, Sema3A significantly inhibits tubule formation of endothelial cells in the Matrigel cultured with starvation medium from SCC-9, compared with the control (p < 0.01). c, a: endothelial cells treated with PBS; b endothelial cells treated with Sema3A; c endothelial cells treated with VEGF; d endothelial cells treated with VEGF plus Sema3A. d, Sema3A significantly inhibits tubule formation of endothelial cells in the Matrigel caused by serum starvation, compared with PBS (p < 0.01); and Sema3A plus VEGF significantly inhibits tube formation of endothelial cells in the Matrigel, compared with VEGF (p < 0.01). e, a CAM treated with PBS; b CAM treated with Sema3A; c CAM treated with VEGF; d CAM treated with Sema3A + VEGF. f, Sema3A significantly increases angiogenesis compared with the control in CAM assay (p < 0.01); however, Sema3A plus VEGF significantly inhibits angiogenesis compared with the VEGF in CAM assay (p < 0.01)