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Cardiovascular Research Advance Access [Accepted Manuscript] published online on April 23, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn097
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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

CSF-1 transfection of myoblasts improves the repair of failing myocardium following autologous myoblast transplantation

Seyedhossein Aharinejad1,2,*, Dietmar Abraham2, Patrick Paulus2, Karin Zins2, Michael Hofmann2, Wolfgang Michlits2, Mariann Gyöngyösi3, Karin Macfelda4, Trevor Lucas2, Karola Trescher4, Michael Grimm1 and E. Richard Stanley5

1 Department of Cardio-Thoracic Surgery, Medical University of Vienna, Waehringerguertel 18-20, A-1090 Vienna, Austria
2 Laboratory for Cardiovascular Research, Department of Anatomy and Cell Biology, Medical University of Vienna, Waehringerstrasse 13, A-1090 Vienna, Austria
3 Department of Cardiology, Medical University of Vienna, Waehringerguertel 18-20, A-1090 Vienna, Austria
4 Center for Biomedical Research, Medical University of Vienna, Währingerguertel 18-20, A-1090 Vienna, Austria
5 Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, NY-10461 New York, USA

* Corresponding Author. Phone: (+431)40400-5620; Fax: (+431)40400-5640. E-mail address: seyedhossein.aharinejad{at}meduniwien.ac.at

Aim: Skeletal myoblasts are used in repair of ischemic myocardium. However, a large fraction of grafted myoblasts degenerate upon engraftment. Colony-stimulating factor-1 (CSF-1) accelerates myoblast proliferation and angiogenesis. We hypothesized that CSF-1 overexpression improves myoblast survival and cardiac function in ischemia-induced heart failure.

Methods and results: Three weeks following myocardial infarction, rats developed heart failure and received intramyocardial injections of mouse CSF-1-transfected or untransfected primary autologous rat myoblasts, recombinant human CSF-1, mouse CSF-1 expressing plasmids, or culture medium. Tissue gene and protein expression was measured by quantitative RT-PCR and Western blotting. Fluorescence imaging and immunocytochemistry were used to analyze myoblasts, endothelial cells, macrophages, and infarct wall thickening. Electrocardiograms were recorded online using a telemetry system. Left ventricular function was assessed by echocardiography over time, and improved significantly only in the CSF-1-overexpressing myoblast group. CSF-1-overexpression enhanced myoblast numbers and was associated with an increased infarct wall thickness, enhanced angiogenesis, increased macrophage recruitment and upregulated matrix metalloproteases (MMP)-2 and -12 in the zone bordering the infarction. Transplantation of CSF-1-overexpressing myoblasts did not result in major arrhythmias.

Conclusion: Autologous intramyocardial transplantation of CSF-1 overexpressing myoblasts might be a novel strategy in the treatment of ischemia-induced heart failure.

Time for primary review: 15 days


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