Fig. 5: MiR-150 reduces cardiac fibrosis as well as the expression of Col5a1 and Col6a1 after myocardial infarction in part by suppressing Sprr1a. | Cell Death & Disease

Fig. 5: MiR-150 reduces cardiac fibrosis as well as the expression of Col5a1 and Col6a1 after myocardial infarction in part by suppressing Sprr1a.

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

Fig. 5

Representative picrosirius red staining (A) from heart sections in the 6 experimental groups at 8 weeks post-MI and fibrosis quantification (B) in whole left ventricles (LVs). Fibrosis histology images from whole heart longitudinal sections (A: Scale bars: 1 mm) are shown. N = 6 per group. Two-way ANOVA with Tukey’s multiple comparison test. ***P < 0.001 vs. sham for each genotype; #P < 0.05 or ###P < 0.001 vs. WT or miR-150 KO. Data are presented as the mean ± SEM. qRT-PCR analysis of profibrotic Col5a1 (C) or Col6a1 (D) expression in 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 change of gene expression normalized to Gapdh. N = 6 per group. Two-way ANOVA with Tukey’s multiple comparison test. **P < 0.01 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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