Cardiospecific deletion of β-catenin gene associated with an activity violation of signaling cascades involved in the development of myocardial hypertrophy

  • O. L. Palchevska Institute of Molecular Biology and Genetics NAS of Ukraine, Ukraine, 03680, Kyiv, 150, Zabolotnoho St.
  • V. V. Balatskyi Institute of Molecular Biology and Genetics NAS of Ukraine, Ukraine, 03680, Kyiv, 150, Zabolotnoho St.
  • L. L. Macewicz Institute of Molecular Biology and Genetics NAS of Ukraine, Ukraine, 03680, Kyiv, 150, Zabolotnoho St.
  • O. O. Piven Institute of Molecular Biology and Genetics NAS of Ukraine, Ukraine, 03680, Kyiv, 150, Zabolotnoho St.


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.

Keywords: β-catenin, hypertrophy, Wnt-signalling, MAPK signalling, PI3-kinase-mTOR-dependent cascade, РКА-signalling, myocardium.


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