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. 2018 Feb 21;9:754. doi: 10.1038/s41467-018-02891-z

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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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Fig. 6 — Myocardial injury activates CM proliferation in neonatal but not adult mice. Neonatal mice underwent left anterior descending artery (LAD) ligation at P1 and clonal analysis performed 21 days post injury. Representative confocal images of a βactin^CreER; R26^VT2/GK, b Nkx2.5^CreER; R26^VT2/GK and c αMHC^CreER; R26^VT2/GK heart (left ventricle) sections. Insets show close-up of boxed regions. d–f Quantification of clonal formation following neonatal injury. LAD ligation was performed in 8-week-old mice (g, h, i), followed by clonal analysis 3 weeks post-injury. Representative fluorescent microscope images of the infarct and border zone of g βactin^CreER; R26^VT2/GK, h Nkx2.5^CreER; R26^VT2/GK and i αMHC^CreER; R26^VT2/GK hearts (left ventricle). j–l Quantification of clonal formation following adult injury. White dashed line marks infarct area. (Tukey’s multiple comparison test), ***p < 0.001 to remote. All measurements shown are depicted as mean ± s.e.m