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. 2018 Feb 13;8:2957. doi: 10.1038/s41598-018-21199-y

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© The Author(s) 2018

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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α-tubulin labelling and co-localisation with JPH2. Confocal images of α-tubulin (magenta) in (a) failing trabeculae and (b) failing ventricle wall, with cell boundaries shown by WGA (grey). (c) Density analysis of α-tubulin labelling at both the tissue and cellular level in the failing tissue sample groups. Tissue density analysis: Trabeculae: n = 14 images, 14 trabeculae, 5 hearts; failing wall n = 15 images, 5 hearts. Cellular density analysis: Trabeculae: n = 24 images, 14 trabeculae, 5 hearts; failing wall n = 27 images, 5 hearts. Data displayed as mean ± SEM. *p = 0.03; ^#p = 0.01. Deconvolved confocal images showing dual labelling with JPH2 (green) in (d) a trabecula and (e) ventricular myocardium from the failing heart. (f) The percentage of JPH2 co-localised with α-tubulin was strongly correlated with increased time-to-peak stress in failing trabeculae (p = 0.017).