Fig. 2: Cardiomyocyte-specific overexpression of GRK−β1AR induces cardiac stress and fibrosis after chronic isoproterenol treatment, which is alleviated by miR-150.
A Representative hematoxylin and eosin (H&E) images from heart sections at 1-week post-treatment show a decrease in abnormal architecture and cellular integrity, and in disorganized structure in ISO GRK−β1AR;miR-150 DTG hearts compared to ISO GRK−β1AR TG controls- Scale bar: 100 μm. B, C Real-Time Quantitative Reverse Transcription (QRT)-PCR analyses of Anp (B) and Tnf-α (C) expression for cardiac damage and inflammation in GRK−β1AR;miR-150 DTG hearts compared to GRK−β1AR TG controls at 1-week post-treatment. N = 6 per group. Data are presented as fold induction of gene expression normalized to glyceraldehyde-3-phosphate dehydrogenase (Gapdh). Two-way ANOVA with Tukey multiple comparison test. ***P < 0.001 vs. vehicle; ###P < 0.001 vs. ISO GRK−β1AR TG. D, E Representative Masson’s trichrome images in heart sections from 4 experimental groups at 1-week post-treatment (D) and fibrosis quantification in whole left ventricles (LVs) (E). Scale bar: 50 μm. N = 6 per group. Two-way ANOVA with Tukey multiple comparison test. ***P < 0.001 vs. vehicle; ###P < 0.001 vs. ISO GRK−β1AR TG. F QRT-PCR analysis of fibrotic Col3a1 expression in GRK−β1AR;miR-150 DTG hearts compared to GRK−β1AR TG controls at 1-week post-treatment. N = 6 per group. Data are presented as fold induction of gene expression normalized to Gapdh. Two-way ANOVA with Tukey multiple comparison test. **P < 0.01 or ***P < 0.001 vs. vehicle; #P < 0.05 vs. ISO GRK−β1AR TG. All data are presented as mean ± SEM.
