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Arrhythmia susceptibility in mice after therapy with beta-catenin-transduced hematopoietic progenitor cells after myocardial ischemia/reperfusion


Gardiwal, A; Reissmann, L M; Kotlarz, D; Oswald, H; Korte, T; Landmesser, U; Klein, G; Templin, C (2009). Arrhythmia susceptibility in mice after therapy with beta-catenin-transduced hematopoietic progenitor cells after myocardial ischemia/reperfusion. Cardiology, 114(3):199-207.

Abstract

BACKGROUND: Hematopoietic progenitor cells (HPCs) can improve cardiac function after myocardial infarction. However, occurrence of arrhythmias is a potential limitation of cell therapy. In this study, we investigated the cardiac electrophysiological properties of ex vivo expanded HPCs, generated by beta-catenin gene transfer, after transcoronary delivery in a murine model of ischemia/reperfusion (I/R) injury. METHODS AND RESULTS: To assess arrhythmia inducibility of ex vivo expanded HPCs, mice were subjected to I/R and assigned to sham operation (n = 8), I/R (n = 21) and HPC (n = 15) treatment. Six weeks later, mice were subjected to long-term electrocardiogram recording and in vivo transvenous electrophysiological study. After I/R, mice showed a significant prolongation of conduction and repolarization compared with sham-operated mice. There was a marked increase in ventricular ectopic activity in infarcted mice as compared with sham-operated mice. Cardiac electrophysiological parameters and ventricular ectopic activity were not altered in mice treated with HPCs in comparison with control I/R mice. CONCLUSION: Transcoronary delivery of genetically ex vivoexpanded HPCs did not alter the electrophysiological properties in mice after I/R. Therefore, ex vivo beta-catenin-mediated HPC expansion may represent an attractive therapeutic option for cell transplantation treatment of myocardial infarction without electrophysiological side effects.

BACKGROUND: Hematopoietic progenitor cells (HPCs) can improve cardiac function after myocardial infarction. However, occurrence of arrhythmias is a potential limitation of cell therapy. In this study, we investigated the cardiac electrophysiological properties of ex vivo expanded HPCs, generated by beta-catenin gene transfer, after transcoronary delivery in a murine model of ischemia/reperfusion (I/R) injury. METHODS AND RESULTS: To assess arrhythmia inducibility of ex vivo expanded HPCs, mice were subjected to I/R and assigned to sham operation (n = 8), I/R (n = 21) and HPC (n = 15) treatment. Six weeks later, mice were subjected to long-term electrocardiogram recording and in vivo transvenous electrophysiological study. After I/R, mice showed a significant prolongation of conduction and repolarization compared with sham-operated mice. There was a marked increase in ventricular ectopic activity in infarcted mice as compared with sham-operated mice. Cardiac electrophysiological parameters and ventricular ectopic activity were not altered in mice treated with HPCs in comparison with control I/R mice. CONCLUSION: Transcoronary delivery of genetically ex vivoexpanded HPCs did not alter the electrophysiological properties in mice after I/R. Therefore, ex vivo beta-catenin-mediated HPC expansion may represent an attractive therapeutic option for cell transplantation treatment of myocardial infarction without electrophysiological side effects.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Cardiology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2009
Deposited On:03 Feb 2010 13:50
Last Modified:01 Jul 2016 14:42
Publisher:Karger
ISSN:0008-6312
Additional Information:© 2010 S. Karger AG
Publisher DOI:10.1159/000228644
PubMed ID:19602881
Permanent URL: http://doi.org/10.5167/uzh-27143

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