Cardiac deletion of α-Е-catenin leads to redused expression of the main component of desmosomes – γ-catenin

  • V. V. Balatskyi
  • L. L. Matsevych
  • O. O. Piven


Aim. In our present work, we have addressed to the γ-catenin, known main component of desmosomes, expression in hearts with heterozygous and homozygous knockout of α-E-catenin gene. Methods. Alpha-E-catenin conditional knockout mice were bred with α-MHC-Cre transgenic mice. We analyze expression of γ-catenin with real time qPCR and Western blot. Results. Cardiac α-E-catenin deletion leads to downregulation of γ-catenin mRNA and protein levels only in homozygous mice, while we not observed any perturbation of γ-catenin expression in heterozygous mice. Conclusions. We have shown that homozygous knockout of α-E-catenin gene in embryonic heart occur reduction of the main component of desmosomes – γ-catenin mRNA and protein level of expression, which can lead to disruption of the desmosomes structure in adult myocardium.

Keywords: α-E-catenin, heart failure, γ-catenin.


Vite A., Radice G.L. N-cadherin/catenin complex as a master regulator of intercalated disc function. Cell. Commun. Adhes. 2014. V. 21. P. 169–179. doi: 10.3109/15419061.2014.908853.

Li J., Radice G.L. A new perspective on intercalated disc organization: implications for heart disease.. Dermatol Res Pract. 2010. V. 2010. P. 207835. doi: 10.1155/2010/207835.

Kostetskii I., Li J., Xiong Y., Zhou R., Ferrari V., Patel V., Molkentin J., Radice G. Induced deletion of the N-cadherin gene in the heart leads to dissolution of the intercalated disc structure.. Circ. Res. 2005. V. 96. P. 346–354. doi: 10.1161/01.RES.0000156274.72390.2c.

Piven O.O., Kostetskii I.E., Macewicz L.L., Kolomiets Y.M., Radice G.L., Lukash L.L. Requirement for N-cadherin-catenin complex in heart development. Exp Biol Med (Maywood). 2011. V. 236. P. 816–822. doi: 10.1258/ebm.2011.010362.

Palchevska O.L., Balatskii V.V., Andrejeva A.O., Macewicz L.L., Piven O.O., Lukash L.L. Embryonically induced β-catenin haploinsufficiency attenuates postnatal heart development and causes violation of foetal genes program. Biopolym. Cell – 2013. V. 29. P. 124–130. doi: 10.7124/bc.00080F.

Balats'kyy V.V., Akymenko I., Matsevych L.L., Piven' O.O., Lukash L.L. Alpha-E-catenin in histological reconstruction of myocardium with aging. Faktory eksperymental'noi evoliutsii orhanizmiv. 2016. V. 18. P. 219–222. [in Ukrainian]

Pluess M., Daeubler G., Dos Remedios C.G., Ehler E. Adaptations of cytoarchitecture in human dilated cardiomyopathy. Biophys. Rev. 2015. V. 7. P. 25–32. doi: 10.1007/s12551-014-0146-2

Li D., Liu Y., Maruyama M., Zhu W., Chen H., Zhang W., Reuter S., Lin S.F., Haneline L.S., Field L.J., Chen P.S., Shou W. Restrictive loss of plakoglobin in cardiomyocytes leads to arrhythmogenic cardiomyopathy.. Hum. Mol. Gen. 2011. V. 20. P. 4582–4596. doi: 10.1093/hmg/ddr392.

Li J., Swope D., Raess N., Cheng L., Muller E.J., Radice G.L. Cardiac tissue-restricted deletion of plakoglobin results in progressive cardiomyopathy and activation of beta-catenin signaling. Mol. Cel. Biol. 2011. V. 31. P. 1134–1144. doi: 10.1128/MCB.01025-10.

Wang T.Y., Wang L., Zhang J.H., Dong W.H. A simplified universal genomic dna extraction protocol suitable for pcr. Genet. Mol. Res. 2011. V. 10. P. 519–525. doi: 10.4238/vol10-1gmr1055.

Gutstein D.E. The organization of adherens junctions and desmosomes at the cardiac intercalated disc is independent of gap junctions. J. Cell Sci. 2003. V. 116. P. 875–885. doi: 10.1242/jcs.00258.

Asimaki A., Syrris P., Wichter T., Matthias P., Saffitz J.E., McKenna W.J. A novel dominant mutation in plakoglobin causes arrhythmogenic right ventricular cardiomyopathy. Am. J. Hum Genet. 2007. V. 81. P. 964–973. doi: 10.1086/521633.