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. 2019 Aug 27;9:12415. doi: 10.1038/s41598-019-48218-w

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© The Author(s) 2019

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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Loss of Jagged1-Notch3 transactivation strength explains the thickening of VimKO arteries. Results of the computational simulation of Notch signaling through arterial layers with parameter variations to investigate the effects of VimKO. The original model parameters are reported in the supplementary material. Average NICD content across the layers, with parameter variations. (A) Changes of Dll1 production have little effects on the average NICD content. (B) Increases of Notch3 production induce higher average NICD contents. (C) Decreases of Jagged-Notch transactivation strength correspond to lower average NICD contents. (D) Similar trends can be observed with respect to the homeostatic number of VSMC layers, computed as the arterial thickness for which the model predicts a switch-type transition from proliferative to contractile VSMC phenotype.