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.
DOI: https://doi.org/10.7124/visnyk.utgis.15.2.877

Abstract

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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