Fig. 5: PKN1 and PKN2 deletion suppresses the differentiation of cardiac fibroblasts after MI.

a Immunofluorescent images of siRNA-treated cardiac fibroblasts immunostained for α-smooth muscle actin (αSMA)-positive stress fibers (green), PDGFRα (red), and nuclei (blue). Quantification of PDGFRα-positive cells (b) and αSMA-positive cells (c) shown as a percentage of DAPI-positive cells (n = 4, biological replicates per group). ns, not significant; ***p = 0.0001; ****p < 0.0001. d Immunofluorescent staining of fibroblasts and myofibroblasts in the cardiac infarction area 7 days after injury. The fibroblasts and myofibroblasts were immunostained for vimentin (red), αSMA (green), and nuclei (blue). e Quantification of vimentin-positive cells shown as a percentage of DAPI-positive cells (n = 6, biological replicates per group). ns, not significant; ****p < 0.0001. f Quantification of dual-positive cells for vimentin and αSMA shown as a percentage of vimentin-positive cells (n = 6, biological replicates per group). ns, not significant; ****p < 0.0001. g Quantification of vimentin-positive cells in the cardiac infarction area 28 days after injury (n = 8, biological replicates per group). ns, not significant; ****p < 0.0001. h Quantification of dual-positive cells for vimentin and αSMA shown as a percentage of vimentin-positive cells 28 days after injury (n = 8, biological replicates per group). ns, not significant; ****p < 0.0001. Data are presented as the mean ± SEM and analyzed using two-way ANOVA followed by Tukey’s post hoc test (b, c, e, f, g, h). The data represent three independent experiments with similar results. Source data are provided as a Source Data file.