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. 2019 Aug 15;9:11893. doi: 10.1038/s41598-019-48174-5

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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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LEAP morphology from hiPSC-derived and primary rodent cardiomyocytes. (a) LEAP repolarization timing is shown for four sources of hiPSC-derived cardiomyocytes. Repolarization is represented as the mean ± standard deviation of APD across wells for APD0 to APD90 (iCell CM2 n = 20 wells, Cor.4U n = 17 wells, Coyne n = 24 wells, Pluricyte n = 5 wells). (b) LEAP repolarization timing is shown for GFP-transfected (n = 17) and Tbx18-transfected (n = 8) primary neonatal rat ventricular cardiomyocytes. (c) Tbx18 transfection altered AP morphology by decreasing APD30 and APD90 relative to GFP-transfection (Mann Whitney U-Test, APD30 p < 0.001, APD90 p < 0.001). (d) GFP-transfected cardiomyocytes exhibited more regular beating than Tbx18 (GFP BP CoV = 8.47 ± 8.50, Tbx18 BP CoV = 39.39 ± 29.23, p < 0.001).