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. 2019 Jul 29;9:11004. doi: 10.1038/s41598-019-47369-0

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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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MC-specific TNFRI does not play a functional role in the activation of MCs and cardiac fibrosis in vivo. (A) Representative flow cytometry scatter plots indicating the percentage of MCs that possess TNFRI, and (B) quantitative flow cytometry analysis of the percentage of MCs possessing TNFRI in left ventricles from wild type mice receiving saline or angiotensin II; (C) Collagen volume fraction for Kit^w-sh/w-sh mice receiving angiotensin II with no BMMCs (n = 7), Kit^w-sh/w-sh mice receiving wild type BMMCs and angiotensin II (n = 7), and Kit^w-sh/w-sh receiving TnfrI^−/− BMMCs and angiotensin II (n = 8); and (D) corresponding representative picrosirius red images. All values are mean ± SEM. *P < 0.05 vs Kit^w-sh/w-sh mice receiving angiotensin II with no BMMCs.