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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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SP does not cause MCs to produce sufficient amounts of pro-fibrotic mediators to influence fibroblast function in vitro, but does increase myofibroblast number in vivo. (A) Tryptase activity in the media of BMMCs treated with SP (n = 4); (B) PCR showing disruption of the PCR product for the NK-R in BMMCs derived from Nk-1r^−/− mice; (C) Hydroxyproline production by 3T3 fibroblasts in response to conditioned media from SP treated BMMCs (n = 15). SP concentrations refer to the treatment of the BMMCs. 10% FBS served as a control. All values are mean ± SEM; *P < 0.05 vs SP 0 nM for (A) and vs 10% FBS for (C). (D) Quantification of α-smooth muscle actin (SMA)⁺ myofibroblasts in LV sections from WKY, SHR, and SHR treated with L732138 (n = 8/group). Values are mean ± SD; ***P < 0.001 vs WKY, ^†p < 0.05 vs SHR; (E) Representative images of α-SMA⁺ myofibroblasts (red = α-SMA). Blue = DAPI nuclear labeling, yellow arrow = blood vessels, white arrow = myofibroblast.