Key result
Cardiospecific heterozygous deletion of β-catenin in mice is associated with increased MAPK and PI3K-mTOR signaling activity but a weaker hypertrophic response to a 6-week swimming test.
p-value: p=<0.05
The transcriptional activity of β-catenin is necessary for the proper interaction of signaling cascades during heart maturation and adaptation to stress.
β-catenin haploinsufficiency weakens hypertrophic response despite enhanced signaling in mice; leaves open its role in human cardiac adaptation.
The aim of our study was to investigate the molecular mechanisms of hypertrophy response under cardiospecific β-catenin haploinsufficiency condition. Materials and methods. Studies were done with β-catenin condtional knockout mice (β-catflox/flox) and α-MHC-Cre-transgenic mice. To induce hypertrophy we used swimming test during 6 weeks. Using western-blot, we have analyzed the level of studied proteins. Results. It has been shown that the β-catenin haploinsufficiency is associated with increased signaling activity of MAPK, PI3-kinase-mTOR-dependent signaling cascades in both: with prolonged physical activity and without it. However, even with an increased activity of this signalling, β-catenin haploinsufficient mice expressed weaker hypertrophic response. Conclusions. The transcriptional activity of β-catenin is necessary for the proper interaction of signaling cascades during heart maturation and adaptation to stress.
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Palchevska et al. (2018) studied Myocardial hypertrophy (n=20). Cardiospecific heterozygous deletion of β-catenin vs. Wild-type mice was evaluated on Signaling activity of MAPK and PI3K-mTOR cascades and hypertrophic response (p=<0.05). Cardiospecific heterozygous deletion of β-catenin in mice is associated with increased MAPK and PI3K-mTOR signaling activity but a weaker hypertrophic response to a 6-week swimming test.
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