13 | 12 | 2017

Embryonically induced cardiospecidic β-catenin deficiency leads to violation of adult heart grows and fetal genes expression 

О.О. Piven1, O.L. Palchevska1,2, V.V. Balatskii1,2, A.O. Andrejeva1,2, L.L. Маcewicz1, L.L. Lukash1 1Іnstitute of Molecular Biology and Genetic 2 Educational and Scientific Centre «Institute of biology» 

One such signalling pathway that plays a major role in both heart development and normal heart homeostasis is the Wnt/β-catenin pathway. In this study we have addressed the role of β-catenin during postnatal heart development and remodelling. Using conditional knockout approach we have studied the significance of cardiospecific developmental ablation of β-catenin for heart development. In our work we analyze how β-catenin haploinsufficiency conditions reflected on postnatal heard development and adult heart formation. Our data demonstrated that β-catenin haploinsufficiency in embryos heart provokes a delay in the development and growth of the adult heart (at 3 month of age) but without any morphological abnormality comparable with controls groups of animals at the same age. At the same time the fetal genes program (ANP, BNP and b-MHC) up-regulation were registered at adult studied groups of animal under β-catenin haploinsufficiency conditions. In our experiment we also registered some age-dependent changes of foetal genes program up-regulation. Namely, with ageing (in 6 month of age animals) we observed that ANP and BNP genes were downregulated but both of hear myosin’s (β- and α-MHC) were overexpressed comparable with control animals. We speculate that cardiospesific β-catenin deficiency leads to destruction of signalling networks in adult heart and as a result can lead to heart violation with ageing, but for this question clarifying its necessary to analyses more older animals.