Fig. 3: Sprr1a knockdown alleviates cardiac apoptosis after myocardial infarction caused by miR-150 deletion. | Cell Death & Disease

Fig. 3: Sprr1a knockdown alleviates cardiac apoptosis after myocardial infarction caused by miR-150 deletion.

From: SPRR1A is a key downstream effector of MiR-150 during both maladaptive cardiac remodeling in mice and human cardiac fibroblast activation

Fig. 3

Representative cleaved caspase-3 staining images in heart sections of the peri-ischemic border area in WT, miR-150 KO, and miR-150 KO;Sprr1ahypo/hypo hearts at 8 weeks post-MI (A) and quantification of apoptosis in six 40X fields (B). Scale bars: 100 μm. qRT-PCR analysis of proapoptotic p53 (C), Bak1 (D), or Bax (E) expression in the ischemic areas from WT, miR-150 KO, and miR-150 KO;Sprr1ahypo/hypo mouse hearts at 8 weeks post-MI. Data are shown as the fold induction of gene expression normalized to Gapdh. N = 6 per group. Two-way ANOVA with Tukey’s multiple comparison test. *P < 0.05 or ***P < 0.001 vs. sham for each genotype; #P < 0.05, ##P < 0.01, or ###P < 0.001 vs. WT or miR-150 KO. Data are presented as the mean ± SEM.

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