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. 2019 Dec 6;9:18545. doi: 10.1038/s41598-019-53867-y

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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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Relaxin signals through Wnt signaling to increase Nav1.5. (A) Less than 10% of untreated myocytes exhibit nuclear β-catenin (Aa,c); however, cells treated with RLX for 24 or 48 hours showed a significant increase in cells positive for nuclear β-catenin (Ab,c). 60x magnification. Data obtained from 3–4 separate preparations, 62–148 cells counted per sample. (B) Cells treated with RLX or CHIR, an inhibitor of GSK3β and Wnt pathway activator, significantly increased Nav1.5 by more than 2-fold (Ba–e, n ≥ 8 cells/group). Inhibition of canonical Wnt signaling by DKK1 blocked the effects of RLX 9 n ≥ 24 cells/group) and Wnt1 (n ≥ 17 cells/group) on Nav1.5 expression (Bf–o). 600x magnification, scale bars = 25 µm and apply to all panels. *Indicates p < 0.05 compared to controls. *Indicates p < 0.05. **Indicates p < 0.01. ***Indicates p < 0.001.