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. 2017 Aug 9;7:7638. doi: 10.1038/s41598-017-07452-w

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© The Author(s) 2017

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Effects of reduced intracellular copper by knocking-down CTR1 or TEPA copper chelation on HMEC-1 angiogenic activity. (a) Representative western blot for CTR-1 protein (35 kDa cropped band) on whole-cell extracts from HMEC-1 cells. GAPDH (37 kDa cropped band) expression was used as a protein loading control. (b) Representative photographs of HMEC-1 cells in Matrigel™ assays. Photographs were taken after knockdown of CTR-1 using 20 nM CTR-1 siRNA B or 8 h incubation with TEPA. Non-silencing siRNA (NSsiRNA) was use as control. Inset, % of inhibition as compared to untreated control cells; N.S. non-significant; Scale bar 200 µM. (c) Total surface area of vascular structure. Columns, n = 3, bars, SEM (****p < 0.0001).