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. 2022 Jan 21;12(1):e693. doi: 10.1002/ctm2.693

FIGURE 2.

FIGURE 2

The absence of miR‐204 promotes pressure overload‐induced CH/CD. (A) The effect of trans‐aortic constriction (TAC)‐induced pressure overload on the expression of miR‐204‐5p in the heart of wild‐type (WT) mice (n = 7–13). (B) Echocardiography‐based assessment of left ventricular weight (LVW) normalised to tibia length (TL) in WT and miR‐204–/– sham/TAC mice (n = 5–10). (C) Representative speckle trackings to measure the cardiac longitudinal strain at systole and diastole. A smaller horizontal green line indicates a higher strain. (D) Quantification of the peak longitudinal strain (%) (n = 5–10). (E) Heart weight (HW) normalised to tibia length (TL) in WT and miR‐204–/– sham/TAC mice (n = 5–10). (F) Expression of hypertrophic markers (nppa, nppb and β‐mhc) in the left ventricle of WT and miR‐204–/– sham/TAC mice (n = 5–10). (G) Representative images showing the effect of miR‐204 absence on cardiac enlargement and fibrosis 5 weeks after sham/TAC surgery. 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 the 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