Key result
Embryonic cardiospecific deletion of the α-E-catenin gene leads to adult heart hypertrophy, accompanied by myocardial fibrosis (2.4% in homozygous knockout) and increased expression of hypertrophic genes.
Why the study?
Does embryonic cardiospecific knockout of α-E-catenin lead to adult heart hypertrophy in mice?
Does embryonic cardiospecific knockout of α-E-catenin lead to adult heart hypertrophy in mice?
Embryonic cardiospecific deletion of α-E-catenin leads to structural myocardial abnormalities and heart hypertrophy in adult mice, indicating its crucial role in maintaining adult heart structure and preventing pathological remodeling.
Answers are grounded in this paper and cite their sources.
Suggests developmental role for α-E-catenin in adult heart structure; hypothesis-generating and leaves open human relevance.
Alpha-Е-catenin is important component of adherent junction in adult myocardium. Early was shown that genetic knockout of this gene during cardiogenesis doesn’t leads to lethality or embryonic heart development violation However, αЕ-catenin role in adult heart development and function is far from understood. Aim of our work is recovering of αЕ-catenin function in heart hypertrophy. In our experiment we have used αЕ-catenin conditional knockout and αMHC-Cre transgenic mice. We have utilized histological methods of analysis: hematoxylin and eosin (H&E), van Gieson staining. The level of hypertrophic genes expression was studied with qPCR. We found that hetero- and homozygous knockout of αЕ-catenin in embryonic heart occur heart hypertrophy in adult mice at 10 months of age, which accompanied by massive histopathological remodelling of heart tissue: fibrosis, infiltration by lymphocytes, nuclear vacuolation, waived cardiomyocytes, vessel walls rapture. Also, the higher levels of hypertrophic genes (ANP and β-MHC) expression were observed in mice with hetero- and homozygous knockout of αЕ-catenin. Thus, hetero- and homozygous deletion of αЕ-catenin is leads to violation of heart tissue structure and hypertrophy in adult heart.
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Balatskyy et al. (2018) studied Heart hypertrophy. Embryonic cardiospecific knockout of α-E-catenin gene vs. Wild-type mice was evaluated on Myocardial fibrosis percentage (p=<0.05). Embryonic cardiospecific deletion of the α-E-catenin gene leads to adult heart hypertrophy, accompanied by myocardial fibrosis (2.4% in homozygous knockout) and increased expression of hypertrophic genes.
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