FIGURE 3.

miR‐204 rescues pressure overload‐induced CH/CD. (A) Cardioselective miR‐204 upregulation by a single injection of AAV9‐miR‐204 (5 × 10¹¹ viral genomes/mouse) 1 week before TAC surgery in miR‐204^–/– mice. Samples were collected 5 weeks after TAC surgery; control mice received the AAV9‐control virus (n = 5). (B) Echocardiography‐based assessment of left ventricular weight (LVW) normalised to tibia length (TL) in miR‐204^–/– TAC mice receiving either AAV9‐miR‐204 or AAV9‐control virus (n = 5). (C) Representative speckle trackings to measure the cardiac longitudinal strain at systole and diastole. A longer horizontal green line indicates a lower strain. (D) Quantification of the peak longitudinal strain (%) (n = 5). (E) Heart weight (HW) normalised to TL in miR‐204^–/– TAC mice receiving AAV9‐miR‐204 or AAV9‐control virus (n = 5). (F) Expression of load‐response genes in the left ventricle of miR‐204^–/– TAC mice receiving AAV9‐miR‐204 or AAV9‐control virus (n = 5). (G) Representative images showing the effect of cardioselective miR‐204 upregulation on cardiac enlargement and fibrosis during TAC. Sirius Red staining shows cardiac fibrosis (brown) at ×20 magnification. (H) Quantification of cardiac fibrosis. n(N) = 25(5). In (H), the replicates are shown as ‘n(N)’, where ‘n’ represents the number of fields and ‘N’ represents the number of mice. Data are shown as mean, and error bars represent SEM. *p < .05, **p < .01, ***p < .001 versus indicated group. nppa, natriuretic peptide a; nppb, natriuretic peptide b; β‐mhc, beta‐myosin heavy chain