Open AccessEmbryonic cardiospecific knockout of α-E-catenin gene leads to alteration of energy metabolism in adult heart
Author(s) -
V. Balatskyy,
L. L. Macewicz,
O. O. Piven
Publication year - 2017
Publication title -
vìsnik. problemi regulâcìï fìzìologìčnih funkcìj/vìsnik kiïvsʹkogo nacìonalʹnogo unìversitetu ìmenì tarasa ševčenka. serìâ: problemi regulâcìï fìzìologìčnih funkcìj
Language(s) - English
Resource type - Journals
eISSN - 2616-6410
pISSN - 1728-2624
DOI - 10.17721/2616_6410.2017.23.65-69
Subject(s) - lipid metabolism , knockout mouse , genetically modified mouse , ampk , biology , endocrinology , western blot , conditional gene knockout , wnt signaling pathway , microbiology and biotechnology , medicine , phosphorylation , catenin , transgene , gene , signal transduction , protein kinase a , biochemistry , phenotype
Previously we have shown that the α-E-catenin knockout in the embryonic heart leads to hypertrophy in adult and activation of canonical Wntsignaling. Heart hypertrophy is also accompanied by metabolic disorders, but role of the α-E-catenin in these processes is not known. Aim of our work is to study the effect of α-E-catenin deletion on the lipid metabolism in the heart. Methods. In our experiment we have used α-Е-catenin conditional knockout and αMHC-Cre transgenic mice. We have utilized histological (Oil Red O staining) and molecular biological (Western blot) methods. Results. α-Е-catenin deletion leads to accumulation of lipid droplets in myocardium, and to violation of expression and phosphorylation of key regulators of lipid metabolism (Ampk, Pparα, Acc, Hsl). Conclusions. Ous results suggest that α-Е-catenin deletion leads to inhibition of lipid metabolism in the heart.