Fig. 9: Impaired epicardial migration in the nkx2.5 loss-of-function model.
From: Activation of Nkx2.5 transcriptional program is required for adult myocardial repair

A–D Myosin Heavy Chain (MHC) immunostaining in injured Tg(tcf21:dsRed) (n = 6) (A, C) and nkx2.5−/−;Tg(hsp70l:nkx2.5-EGFP);Tg(tcf21:dsRed) (n = 5) (B, D) at 14 dpa exhibits aborted epicardial penetration in the nkx2.5−/− heart. Scale bar, 50 μm. E EPDC migration quantification strategy measures the distance from the apex of the heart to the maximal interior position of the Tcf21:DsRed2+ cells in injured wild-type (n = 6) and nkx2.5−/− (n = 5) hearts (A–D). Mean and standard error of each data set are shown. Unpaired, two-tailed t-test demonstrates a statistically significant difference between WT14 and MT14 (p = 0.0035). F, G Ex vivo epicardial migration assay in Tg(tcf21:dsRed) (n = 14) (G) and nkx2.5−/−;Tg(hsp70l:nkx2.5-EGFP);Tg(tcf21:dsRed) (n = 14) (H) explants. H, I Quantification of the epicardial migration showing no statistical difference between the wild-type (n = 14) and the nkx2.5−/− (n = 14) cultured apices (F, G). Additional quantification of Edu+tcf21:dsRed+ cells indicates normal proliferative potential in cultured nkx2.5−/− (n = 14) versus wild-type epicardium (n = 12) (J, K). Mean and standard error of each data set are shown with no statistically significant differences detected by unpaired, two-tailed t-tests between WT and MT (p = 0.8794 in H and p = 0.6165 in I). J, K Edu proliferation assay in wild-type (n = 12) (K) and nkx2.5−/− (n = 14) (L) epicardial tcf21:dsRed+ cells. Scale bar, 50 μm. Source data are provided as a Source Data file.