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. 2016 Apr 21;1(5):e85923. doi: 10.1172/jci.insight.85923

Figure 9. Dsg2 mutant mice with constitutively active GSK3β demonstrate increased myocardial fibrosis and cardiac dysfunction.

Figure 9

(A) Representative short-axis, m-mode echocardiography from WT and heterozygous and homozygous Dsg2 mutant mice with 1 or 2 copies of mutant GSK3β-S9A alleles. Images are representative of n ≥ 4/genotype. (B) Quantitative echocardiography analysis of WT and heterozygous and homozygous Dsg2 mutant mice expressing 1 or 2 copies of mutant GSK3β-S9A at 4, 8, and 16 weeks of age. Mean ± SEM, n ≥ 4/genotype/time point. *P < 0.05 for Dsg2mut/mut; GSK3βS9A/+ and Dsg2mut/mut; GSK3βS9A/S9A vs. WT using 2-way ANOVA with Tukey’s post-hoc analysis. (C) Representative images of ventricular myocardia from WT, heterozygous, and homozygous Dsg2 mutant mice with either 1 or 2 copies of mutant GSK3β-S9A stained with Masson’s trichrome (MTC). Images are representative of n = 4/genotype. Scale bar: 1 mm.