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. 2016 Jul 20;6(7):160101. doi: 10.1098/rsob.160101

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© 2016 The Authors.

Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

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Figure 3. — Thoracotomy triggers the remodelling of the heart architecture. (a,b) Uninjured and 30 dpt heart sections of transgenic zebrafish cmlc2:DsRed2-nuc (red) after one month of BrdU treatment (green). (c,d) Representative sections of hearts labelled with Phalloidin (red), a muscle marker, at 30 dpt. (e) Representative section of an uninjured heart labelled with haematoxylin/eosin (h,e) staining. Compact myocardium (Comp. MC) is composed of a dense layer of CMs, surrounding the trabecular myocardium (Trab. MC) with a spongy lumen. (a–e) Dashed lines separate compact and trabecular myocardium. (f,g) Percentage of BrdU-positive CMs in whole myocardium (f) or in the two distinct myocardium compartments (g). (h–j) Morphometric measurements of hearts at 30 dpt. No difference in heart size was noticed (h), but a thickening of the compact myocardium was observed (i). (j) The density of CMs (number of CMs per 10 000 µm² of cardiac muscle) is higher at 30 dpt in comparison to uninjured control (n ≥ 4 hearts; ≥2 sections per heart; *p < 0.05; ***p < 0.001).