Fig. 3 | Signal Transduction and Targeted Therapy

Fig. 3

From: The double face of miR-320: cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction

Fig. 3

Overexpression of miR-320 in CMs aggravated HF in vivo. a Relative miR-320 expression in isolated CMs measured by real-time PCR. b Representative gross morphologies of hearts from mice subjected to different treatments. c The ratios of heart weight to body weight in mice with diverse treatments. d Representative images of transverse area of CMs detected by H&E. Scale bars, 50 µm. e Histological analysis of transverse area of CMs measured by WGA staining (left). Scale bars, 25 µm. The areas of CMs were analyzed by Image-Pro Plus (right). f Echocardiography analysis of LVEF%, LVFS%. g Hemodynamic parameters (dp/dtmax and dp/dtmin) were measured by the Millar cardiac catheter system. h Relative mRNA expressions of cardiac hypertrophy markers in heart tissues from treated mice. i Representative images of Sirius Red staining of heart sections from mice with different treatments (left), and the quantification analysis of cardiac fibrosis (right). Scale bars, 50 µm. H&E hematoxylin and eosin, WGA wheat germ agglutinin. Sham (n = 9), TAC + NS (n = 8), TAC + rAAV9-TNT-GFP (n = 8), TAC + rAAV9-TNT-miR-320 (n = 8), TAC + rAAV9-TNT-miR-320-TUD (n = 8). Data are expressed as mean ± SEM

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