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Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice

  • Molecular and cellular mechanisms of disease
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A Correction to this article was published on 04 July 2018

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Abstract

αE-catenin is a component of adherens junctions that link the cadherin-catenin complex to the actin cytoskeleton. The signaling function of this protein was recently revealed. In the present study, we investigated the role of αE-catenin in the pathogenesis of heart failure. We mated αE-catenin conditional knockout mice with αMHC-Cre mice and evaluated their mutant offspring. We found that αE-catenin knockout caused enlargement of the heart and atria, fibrosis, the upregulation of hypertrophic genes, and the dysregulation of fatty acid metabolism via the transcriptional activity of Yap and β-catenin. The activation of canonical Wnt and Yap decreased the activity of main regulators of energy metabolism (i.e., adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor α) and dysregulated hypertrophic pathway activity (i.e., phosphatidylinositide 3-kinase/Akt, cyclic adenosine monophosphate/protein kinase A, and MEK1/extracellular signal regulated kinase 1/2). The loss of αE-catenin also negatively affected cardio-hemodynamic function via the protein kinase A pathway. Overall, we found that the embryonic heart-specific ablation of αE-catenin leads to the development of heart failure with age and premature death in mice. Thus, αE-catenin appears to have a crucial signaling function in the postnatal heart, and the dysfunction of this gene causes heart failure through canonical Wnt and Yap activation.

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  • 04 July 2018

    The original version of this article unfortunately contained a mistake. The published paper presented an incorrect version of Table 1. The corrected Table is given here.

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Acknowledgements

We thank Dr. Glenn Radice, Thomas Jefferson University, for providing αMHC-Cre and αE-catenin animals. We also thank Lesya V. Tumanovska, MSc, Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, for assistance with the cryosection preparations. This study was supported by a Joint Research Project under a scientific cooperation agreement between the Polish Academy of Science and National Academy of Sciences of Ukraine (2015-2017). OOP was supported by the National Academy of Sciences of Ukraine (N40/2015-2020). PD and AMG were supported by grants from the National Science Centre, Poland (UMO-2014/13/B/NZ4/00199, UMO-2016/22/E/NZ4/00650, and UMO-2015/17/D/NZ5/03446). VN was supported by the European Union’s Horizon 2020 research and innovation program under Marie Sklodowska-Curie grant agreement no. 665735 (Bio4Med) and by funding from the Polish Ministry of Science and Higher Education as part of 2016-2020 funds for the implementation of international projects (agreement no. 3548/H2020/COFUND/2016/2).

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Authors and Affiliations

  1. Department of Human Genetics, Institute of Molecular Biology and Genetics, National Academy of Sciences of Ukraine, 150 Akad. Zabolotnogo str, Kyiv, 03680, Ukraine

    Volodymyr V. Balatskyi, Larysa L. Macewicz & Oksana O. Piven

  2. Laboratory of Molecular Medical Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur str, 02-093, Warsaw, Poland

    Ana-Maria Gan, Viktor O. Navrulin, Adam Olichwier & Pawel Dobrzyn

  3. Department of General and Molecular Pathophysiology, Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, 4 Bogomoletz str, Kyiv, 01024, Ukraine

    Sergii V. Goncharov, Georgiy V. Portnichenko, Tetiana Yu Lapikova-Bryginska & Victor E. Dosenko

  4. Laboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur str, 02-093, Warsaw, Poland

    Paulina Pawelec

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  1. Volodymyr V. Balatskyi
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Contributions

All of the authors participated in the design of the study and interpretation and analysis of the data and reviewed of the manuscript. PD, VD, and OOP planned the experiments, discussed the results, and wrote the manuscript. VVB and LLM were involved in the generation of transgenic mice and genotyping, conducted the morphological analysis, performed qPCR, and performed the statistical analysis. AMG, PP, VON, and AO performed the protein isolation and Western blot analysis. SG, GP, and TLB measured and statistically analyzed the cardio-hemodynamic parameters.

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Correspondence to Oksana O. Piven.

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Balatskyi, V.V., Macewicz, L.L., Gan, AM. et al. Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice. Pflugers Arch - Eur J Physiol 470, 1485–1499 (2018). https://doi.org/10.1007/s00424-018-2168-2

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