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0219U100867,
0115U002949
,
The study of the regulatory functions of b - and a-catenin in age and patological reconstruction of the adult myocardium to the needs of personalized medicine and the development of modern methods of prevention, disease diagnosis and treatment of heart diseases
Piven Oksana O., Кандидат біологічних наук
22-03-2019
Institute of Molecular Biology and Genetics of NAS of Ukraine
Hypertrophy of the myocardium is its adaptation to the physical. Hormonal and other stresses. One of the mechanisms for such an adaptation is the heart embedment. This process occurs both on the morphological and molecular genetic levels. Among the series of signaling cascades involved in controlling the adaptation of the heart to hypertrophic loads is the canonical Wnt signaling cascade. In our work, we have shown that the proteins of intercellular adhesion b-catenin and aE-catenin are not only of fundamental importance in the formation of tissue of rye but also involved in control of proliferation, terminal differentiation of newborn cardiomyocytes. We were first shown that aE-catenin has not only an important function in maintaining intercellular adhesion, but also signaling. Namely, aE-catenin is a suppressor of transcriptional activity of b-catenin and Yap in neonatal cardiomyocytes. The deletion of the aE-catenin gene leads to an increase in the sinus activity of b-catenin and Yap, which leads to increased proliferative activity of the cardiomyostats, hypoplasia and enlargement of the newborn's myocardium, but is accompanied by a delay in the terminal differentiation of the heart cells. On the other hand, the violation of the activity of the cannonal Wnt signaling cascade as a result of heterozygous knockout of the b-catenin gene also caused a violation of heart formation and proliferation of neonatal cardiomyocytes. Thus, homo- and heterozygous knockout of the b-catenin gene leads to a violation of the activity of the cannonal Wnt signaling (increased expression of TSCF-4, Axin2, c-Fos and CyclinD2 genes) in the postnatal myocardium, and as a consequence, suppresses the proliferative activity of cardiomyocytes, decreases heart size, hypoplasia. Also, such violations led to a delay in terminal differentiation of neonatal cardiomyocytes, namely, a decrease in the number of dual-core cardiomyocytes and an increase in the expression of the fetal gene of the ANP
Matsevych Larysa L.
2020-04-02
Updated: 2025-12-08
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