Fig. 1: Sprr1a knockdown attenuates cardiac dysfunction after myocardial infarction mediated by miR-150 loss. | Cell Death & Disease

Fig. 1: Sprr1a knockdown attenuates cardiac dysfunction after myocardial infarction mediated by miR-150 loss.

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

Fig. 1

Transthoracic echocardiography was performed on the 6 experimental groups (sham and MI of WT, miR-150 KO, and miR-150 KO;Sprr1ahypo/hypo) at 0, 3 days, 4 weeks, and 8 weeks post-MI. Quantification of the left ventricular (LV) ejection fraction (EF: A), fractional shortening (FS: B), end-diastolic volume (LVEDV: C), end-systolic volume (LVESV: D), internal diameter, diastole (LVIDd: E), and internal diameter, systole (LVIDs: F) is shown. N = 10–21 per group. Two-way repeated-measures ANOVA with Bonferroni post hoc test for 2 groups over time. **P < 0.01 or ***P < 0.001 vs. sham for each genotype (denoted by different colors for sham within same group); #P < 0.05 or ##P < 0.01 vs. MI WT (denoted by blue); and §§P < 0.01 or §§§P < 0.001 vs. MI miR-150 KO (denoted by brown). Data are presented as the mean ± SD.

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