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. 2016 Aug 30;26(10):1099–1111. doi: 10.1038/cr.2016.101

Figure 5.

Figure 5

CRISPR/Cas9-mediated genome editing improves the heart function of PRKAG2 cardiac syndrome in transgenic mouse model. (A-E) Continuous measurement of LV wall thickness (A), the thickness of IVS (B), LV diastolic diameter (C), LV fractional shortening (D), and LV ejection fraction (E) by echocardiography. Two-way ANOVA was used to analyze overall differences between all groups (n = 31, 19, and 20 for control, AAV9-EGFP, and AAV9-Cas9/sgRNA-1-treated Tg-H530R mice, respectively, at age of 4 weeks; n = 28, 18, and 18 at age of 8 weeks; n = 18, 17, and 14 at age of 12 weeks; n = 18, 16, and 13 at age of 16 weeks; n = 14, 14, and 11 at age of 20 weeks; n = 12, 11, and 9 at age of 24 weeks, respectively). Unpaired two-tailed Student's t-test was performed for single comparison between AAV9-EGFP and AAV9-Cas9/sgRNA-1-treated Tg-H530R mice (*P < 0.05, **P < 0.01, ***P < 0.001). (F) Lead II electrocardiogram. (G) Incidence of pre-excitation of 12-week-old control, AAV9-EGFP and AAV9-Cas9/sgRNA-1-treated Tg-H530R mice.