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. 2017 Jan 23;18:10. doi: 10.1186/s12860-017-0127-y

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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 — TGF-β1 induced reduction in endothelial cord formation occurs via an ALK5 related pathway. a Representative phase contrast images showing endothelial cell cord formation 8 h after plating on Matrigel™ under control conditions (C; DMSO vehicle), 5 μM SB-431542 (an ALK5 inhibitor) in DMSO (SB), 5 ng/ml exogenous TGF-β1 (T) or 5.0 ng/ml TGF-β1 plus 5 μM SB-431542 (T + SB). b WimTube automated quantification of cord formation showed SB inhibitor significantly blocked the ability of 5.0 ng/ml TGF-β1 to significantly inhibit total cord length, cord branching, formation of loops, and generation of tip cells. SB inhibitor, either alone or in combination with 5.0 ng/ml TGF-β1 was not significantly different from DMSO control. **p ≤ 0.01; ***p ≤ 0.001; N = 4; Kruskal-Wallis test