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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: J Mol Cell Cardiol. 2019 May 11;132:84–97. doi: 10.1016/j.yjmcc.2019.05.006

Figure 2: Smad2 is activated in infarct myofibroblasts.

Figure 2:

Dual immunofluorescence combining pSmad2 staining and α-SMA labeling (to label infarct myofibroblasts as spindle shaped α-SMA+ cells located outside the vascular media) was used to identify myofibroblasts exhibiting Smad2 activation. In control (c) hearts (A, B) α -SMA immunoreactivity was localized exclusively in vascular mural cells (arrowheads) and levels of pSmad2 staining were very low. C: After 7 days of permanent coronary occlusion, abundant myofibroblasts in the infarct zone (7DI) exhibited activation of Smad2 signaling, evidenced by nuclear localization of pSmad2 (arrows, C). D: Relatively few myofibroblasts (arrowheads) were noted in the remote remodeling myocardium (7DR) and had negligible pSmad2 expression. E: Quantitative analysis shows that the density of p-Smad2+ myofibroblasts in healing infarcts peaked after 7 days of permanent coronary occlusion. (****p<0.0001 vs. sham, n=4–6/group – Kruskall-Wallis non-parametric ANOVA followed by Dunn’s multiple comparison post-test). Scalebar=20 μm