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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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The NK-1R increases SCF production, but does not alter MC proliferation or apoptosis. (A) Stem cell factor levels for SHR, WKY, and SHR treated with the NK-1R antagonist L732138 (5 mg/kg/d). All values are mean ± SEM; n = 6–8; ***P < 0.001, ****P < 0.0001; (B) In situ hybridization identifying cells expressing SCF (antisense) in the left ventricle. Endothelial cells and cardiomyocytes labeled positive for stem cell factor (black arrows). Incubation with sense probes served as the negative control; (C) Flow cytometry analysis of BMMCs (FcεRI⁺ cells) indicating that 95% of BMMCs possess the NK-1R; (D) c-kit protein levels on BMMCs as determined by ELISA; (E) BMMC proliferation assay (n = 12); Quantification of cleaved caspase-3 (F) and apoptosis inducing factor (AIF) (G); Representative western blots for cleaved caspase-3 and AIF (H) from BMMCs treated with SP (n = 6). All values are mean ± SEM. Gel images in (D) are cropped from three separate blots. Images of full-length blots are included in Fig. S7.