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. 2014 Nov 16;15:178. doi: 10.1186/1471-2369-15-178

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© Wang et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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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TL1A induced NF-κB activation in vascular endothelial cells in mouse heart organ cultures. (6a) Heart tissue from DR3 wild type (wt) and DR3 knock-out (ko) mice were treated with TL1A or TNF and immunolabeled as described in materials and methods. DR3wt showed more nuclear NF-κB activation in CD31 positive EC after TL1A treatment (B) compared to the untreated (A). There was similar odd nuclear NF-κB activation in DR3ko mice EC between TL1A treated (E) and untreated cultures (D). TNF induced a more profound nuclear NF-κB activation in EC of both DR3wt and DR3ko (C and F). Results were representative of 3 experiments. (6b) Graph showed a statistical difference in number of EC in TL1A treated tissue with NF-κB activation in DR3wt compared to DR3ko (p < 0.05) (*).