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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: J Mol Cell Cardiol. 2015 Oct 19;89(Pt B):287–296. doi: 10.1016/j.yjmcc.2015.10.018

Figure 1.

Figure 1

Representative confocal images and quantitation of Wnt signaling and CM proliferation gradients in the ventricular wall of normal E13.5 embryos. A and B, β-catenin is stronger at the compact (Com) than trabecular (Tra) layer and quantitation of average β-catenin intensity (B, bar graph) in Actinin positive CMs that contain membranous and nuclear β-catenin (B). C and D, Ki67 gradient with low power view (C) and double labeling with sarcomeric α-actinin (Actinin, D) and quantitation of percentage of Ki67 (bar graph) positive CMs in Com and Tra layers. E and F, APC decorates Actinin positive CMs, but not Actinin negative endothelial cells (triangles) and quantitation shows higher APC intensity in Tra than in Com layer. G, An illustration (left) shows how nuclear β-catenin intensity was measured for entire images as well as bar graphs demonstrate average nuclear β-catenin intensity in Com and Tra layers. Regions of interest (ROIs) are semi-automatically outlined by image J based on all Actinin positive areas. H, A diagram illustrates that β-catenin is expressed at the highest levels in the rapidly proliferating compact myocardium, forming a decreasing intensity gradient from the epicardium to the endocardium. In contrast, APC shows the strongest expression at the slowly proliferating trabecular layer form an increasing intensity gradient from the epicardium to the endocardium. Dotted lines show visceral pericardium and bars=50μm. Data represent mean ± SD. N=3-4 independent experiments.