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. 2021 Jan 1;11(3):1249–1268. doi: 10.7150/thno.48787

Figure 1.

Figure 1

Cardiomyocyte-specific overexpression of LRP6 prevents cardiac dysfunction induced by pressure overload. (A), Echocardiographic analysis of fraction shortening (FS) in mice at different time-points (3d, 1w, 2w, and 4w) after TAC. *p < 0.05 vs Sham group; n = 6-10 mice/each group. (B), Western blot analysis of p-LRP6 and LRP6 levels in left ventricular tissues from mice at different time-points (3d, 1w, 2w, and 4w) after TAC. *p < 0.05; **p < 0.01 vs sham group; n = 4 mice/ each group. (C), Summary of the generation of tamoxifen-inducible cardiac-specific LRP6 overexpressing mice. (D), Representative images of Western blot analysis of LRP6 expression in heart and kidney tissues from LRP6CAG/MCM after injection of tamoxifen or DMSO for 3 consecutive days. (E), Representative images of Western blot analysis of LRP6 expression in isolated CMs and non-CMs from tamoxifen-injected LRP6CAG/MCM (LRP6 Over) or -MCM (MCM) mice. CMs: cardiomyocytes. (F), Overall strategy of exploring the effects of cardiac LRP6 overexpression in TAC mice. (G), Echocardiographic analysis of cardiac function in tamoxifen-injected LRP6CAG/MCM (LRP6 Over) or -MCM (MCM) mice at 2 weeks and 4 weeks after TAC or sham operation. FS: fraction shortening; EF: ejection fraction; LVID;d: left ventricular diastolic internal diameter. HR: heart rate; *p < 0.05; **p < 0.01; n = 7-12/each group.