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- W2277496552 abstract "Introduction Cell-cell contact proteins including plakoglobin (γ-catenin, plako) play a critical role in the pathogenesis of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). Development of the ARVC phenotype has been shown to be accelerated by endurance training. In swim-trained heterozygous plako-deficient (plako+/-) mice with an ARVC phenotype comprised of arrhythmias and right ventricular dilation, expression of the gap junction protein connexin43 (Cx43) was found to be pronouncedly decreased. This was associated with functional conduction block and a reduction in longitudinal conduction velocities. However, it is unclear if junctional protein changes other than plako deficiency itself exist prior to ARVC disease onset in plako deficiency. Purpose To investigate the specific expression of plako, β-catenin (a structural homologue of plako), and Cx43 in left and right ventricles (LV and RV) from young sedentary asymptomatic plako+/- mice. Methods Echocardiography was performed on anaesthetised 19-week-old littermate plako+/- and wildtype (WT) mice (n = 21–22). Freshly-prepared LV and RV samples (5 per genotype for each ventricle) were snap-frozen and protein expression quantitatively assessed using SDS-PAGE/Western blotting. All experiments were blinded to genotype. Results ARVC phenotype was not apparent at this stage, as reflected by normal RV size (e.g. diastolic diameter: plako+/- 1.60 ± 0.03 mm vs WT 1.65 ± 0.03 mm). Plako expression was decreased in plako+/- hearts compared to WT for both LV (plako+/- 0.06 ± 0.01 vs WT 0.08 ± 0.01; p Conclusions β-catenin expression is increased in LV and RV of young sedentary plako+/- mice with confirmed deficiency of plako protein expression. This may reflect a compensatory response to the reduced levels of plako. Our results suggest that Cx43 expression is not critically down-regulated prior to ARVC disease onset." @default.
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- W2277496552 date "2015-06-01" @default.
- W2277496552 modified "2023-09-27" @default.
- W2277496552 title "YIA5 Plakoglobin Deficiency Leads to Increased Biventricular Beta-Catenin Expression in the Murine Heart" @default.
- W2277496552 doi "https://doi.org/10.1136/heartjnl-2015-308066.228" @default.
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