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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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RyR co-localisation with JPH2 is altered in human HF. Deconvolved confocal micrographs showing RyR (red) and JPH2 (green) dual labelling in (a) a trabecula and (b) ventricle wall sample from failing hearts. (c) Co-localisation analysis reveals the extent of RyR co-localised with JPH2 and JPH2 co-localised with RyR in the trabeculae and ventricle wall from failing human hearts. (d) Tissue labelling density revealed no differences for RyR or JPH2. (e) A positive relationship is observed between JPH2 tissue density and peak stress development (normalised to MCSA) in trabeculae from the failing human heart (p = 0.041). (f) JPH2 tissue labelling density forms a strong, positive relationship with the percentage of RyR clusters associated with t-tubules (tt) in failing human trabeculae (p = 0.0014). Co-localisation analysis: Trabeculae: n = 21 images, 14 trabeculae, 5 hearts; failing wall n = 22 images, 5 hearts. Density analysis: Trabeculae: n = 14 images, 14 trabeculae, 5 hearts; failing wall n = 14 images, 5 hearts. Data displayed as mean ± SEM.