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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. 5 — TGF-β1 reduces VEGFR2 expression via multiple mechanisms. a Western blot showing TGF-β1 induced loss of cell associated VEGFR2 protein and concomitant increase in full-length VEGFR2 detected in conditioned medium. b Quantitative PCR analysis showed that there was no change in the relative ratio of full length VEGFR2 mRNA to alternative spliced sVEGFR2 mRNA upon TGF-β1 treatment. c TGF-β1 treatment induced increased expression of ADAM family sheddase enzyme ADAM 10. TGF-β1 treatment had no effect on the expression of ADAM 17 or the membrane-associated metalloproteinase MMP-14. d Ultracentrifugation of endothelial conditioned medium demonstrated that soluble VEGFR2 is associated with the extracellular vesicle/exosome marker HSP90 in TGF-β1 treated cells