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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. 4 — TGF-β1 induced reduction in receptor expression occurs via an ALK5 related pathway. a) Representative western blots and densitometry (b) from BAEC exposed to 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) for 24 h. TGF-β1 leads reduced VEGFR2 expression and activation, and significantly upregulated endoglin in an ALK5/SMAD2-dependent fashion (as revealed by pSMAD2). There were no significant changes in SMAD1/5-dependent signaling, or in VEGFR1, Notch1 or Dll4 expression. *p ≤ 0.05; N = 3; Kruskal-Wallis test