fig1

Pharmacological suppression of the WNT signaling pathway attenuates age-dependent expression of the phenotype in a mouse model of arrhythmogenic cardiomyopathy

Figure 1. Suppression of the canonical WNT in the wild type and Myh6-Cre:DspW/F (cardiac myocyte-specific heterozygous deletion of the Dsp gene) mice. (A) Transcript levels of Axin2, a bona fide target of the cWNT pathway in the wild type and Myh6-Cre:DspW/F mice treated with placebo and WNT974 along with untreated controls, as determined by RT-PCR. Relative fold change in the transcript levels was determined by comparing all the groups to the wild type untreated group. (N = 5-7 per group). (B) Representative immunofluorescence images depicting expression and nuclear localization of TCF7L2 protein, a co-transcriptional regulator of the canonical WNT pathway, in the myocardial sections in the experimental groups. (C) Quantitative data showing the percentage of cells expressing TCF7L2 in the myocardial sections in the experimental groups. The P values were determined by the student t-test between two groups and genotype-by-treatment interactions were determined by 2-way ANOVA. The significant P values (< 0.05) between the groups are presented. PG: P value for the effect of the genotype; PTr: P value for the effect of treatment; Pi: P value for treatment-by-genotype interaction.

The Journal of Cardiovascular Aging

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