Fig. 1: Cardiomyocyte-specific overexpression of GRK−β1AR exacerbates cardiac dysfunction following chronic isoproterenol treatment, which is in part rescued by miR-150. | Cell Death Discovery

Fig. 1: Cardiomyocyte-specific overexpression of GRK−β1AR exacerbates cardiac dysfunction following chronic isoproterenol treatment, which is in part rescued by miR-150.

From: MiR-150 blunts cardiac dysfunction in mice with cardiomyocyte loss of β1-adrenergic receptor/β-arrestin signaling and controls a unique transcriptome

Fig. 1

A MiR-150 expression in left ventricles (LVs) from cardiomyocyte (CM)-specific GRK−β1AR transgenic (TG) and GRK−β1AR;miR-150 double TG (DTG) mice at 1 week after vehicle or isoproterenol (ISO) infusion. N = 6. Data are presented as fold induction of miR-150 expression normalized to U6 snRNA. Two-way ANOVA with Tukey multiple comparison test. **P < 0.01 or ***P < 0.001 vs. vehicle; ##P < 0.01 or ###P < 0.001 vs. GRK−β1AR TG. B–F Transthoracic echocardiography was performed in 4 experimental groups (vehicle and ISO of GRK−β1AR TG and GRK−β1AR;miR-150 DTG) at week 0 and 1 post-treatment. Quantification of LV ejection fraction (B), fractional shortening (C), internal diameter, systole (LVIDs: D), anterior wall thickness, diastole (LVAWd: E), and posterior wall thickness, diastole (LVPWd: F) is presented. N = 18 per group. Two-way repeated-measures ANOVA with Bonferroni post hoc test. ***P < 0.001 vs. vehicle; ##P < 0.01 or ###P < 0.001 vs. GRK−β1AR TG. All data are presented as mean ± SEM.

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