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Cardiovascular Research Advance Access originally published online on October 11, 2008
Cardiovascular Research 2009 81(1):108-115; doi:10.1093/cvr/cvn276
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Proapoptotic protein Siva binds to the muscle protein telethonin in cardiomyocytes during coxsackieviral infection

Katharina Mihatsch1, Matthias Nestler2, Hans-Peter Saluz1, Andreas Henke3 and Thomas Munder1,*

1 Department of Cell and Molecular Biology, Leibniz Institute for Natural Product Research and Infection Biology e. V. – Hans Knöll Institute, Beutenbergstr. 11a, D-07745 Jena, Germany
2 Department of Biomolecular NMR Spectroscopy, Leibniz Institute for Age Research e. V. – Fritz Lipmann Institute, Beutenbergstr. 11a, D-07745 Jena, Germany
3 Institute of Virology and Antiviral Therapy, Medical Center, Friedrich Schiller University Jena, Hans Knöll Str. 2, D-07745 Jena, Germany

* Corresponding author: Department of Medical Engineering and Biotechnology, University of Applied Sciences Jena, Carl-Zeiss-Promenade 2, D-07745 Jena, Germany. Tel: +49 36 41 205 660; fax: +49 36 41 205 601. E-mail address: thomas.munder{at}fh-jena.de

Aims: Coxsackievirus B3 (CVB3) is known to cause a variety of human diseases including acute and chronic myocarditis as well as dilated cardiomyopathy (DCM). However, the mechanisms by which CVB3 causes diseases are not well understood.

Methods and results: Studies identifying protein–protein interactions during CVB3 infection are useful in delineating the pathogenesis of acute or chronic myocarditis. Screening a human heart cDNA library revealed a yet unknown interaction partner of the proapoptotic protein Siva. We demonstrate that Siva specifically interacts with the heart and skeletal muscle protein telethonin. The expression of Siva is increased in heart tissue of CVB3-infected mice and the proteins colocalize in cardiomyocytes.

Conclusion: telethonin might be involved in CVB3-mediated cell damage and in the resulting cardiac dysfunction due to the interaction with Siva. We suggest a molecular mechanism through which coxsackieviral infection contributes to the pathogenesis of chronic myocarditis and in particular of acquired forms of DCM.

KEYWORDS Cardiomyocytes; Colocalization; Coxsackievirus B3; Siva; Telethonin

Time for primary review: 41 days


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