alexa Functional Exhaustion of Bone Marrow Derived Endothelial Progenitor Cells in a Chronic Swine Model of Myocardial Ischemia
ISSN: 2161-0479

Journal of Autacoids and Hormones
Open Access

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Special Issue Article

Functional Exhaustion of Bone Marrow Derived Endothelial Progenitor Cells in a Chronic Swine Model of Myocardial Ischemia

Simon Maltais1,3, Nicholas A Haglund3, Jean Francois Tanguay2, Martin G Sirois2, Jean Claude Tardif2, Louis P Perrault1, Hak Joon Sung4 and Hung Q Ly2*
1Department of Cardiac Surgery
2Department of Medicine, Montreal Heart Institute, University of Montreal, Montreal, Quebec, Canada
3Department of Cardiac Surgery and Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA
4Department of Biomedical Engineering, Vanderbilt University Medical Center, Nashville, Tennessee, USA
*Corresponding author: Hung Q. Ly, MD, MSc, FRCPC
Department of Medicine
Montreal Heart Institute
University of Montreal
5000 Belanger St East, Montreal
Quebec, H1T 1C8, Canada
Tel: 514-376-3330
Fax: 514-376-6299
E-mail: [email protected]
Received November 24, 2011; Accepted January 09, 2012; Published January 12, 2012
Citation: Maltais S, Haglund NA, Tanguay JF, Sirois MG, Tardif JC, et al. (2011) Functional Exhaustion of Bone Marrow Derived Endothelial Progenitor Cells in a Chronic Swine Model of Myocardial Ischemia. Autacoids S3:002. doi:10.4172/2161-0479.S3-002
Copyright: © 2011 Maltais S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

The functional impairment of bone marrow derived endothelial progenitor cells remains an important barrier for cardiac cell-based therapies. Our aim was to create a relevant swine model of chronic ischemia and document its effect on bone derived progenitor cells. We hypothesized that bone marrow derived endothelial progenitor cells would be functionally impaired in the setting of chronic cardiac dysfunction of ischemic origin. At baseline, Landrace miniswine was instrumented with a fixed occluder to the proximal left anterior descending coronary artery. We evaluated the animals over a 3-month period (0, 45 and 90 days). Focal proximal left anterior descending stenosis was angiographically confirmed in all animals (mean diameter stenosis = 96±4%, n=12). The resulting ischemic myocardium had evidence of contractile dysfunction but preserved viability. A progressive decline in circulating levels of endothelial progenitor cells was documented 3 months following instrumentation (P<0.001). Quantitative polymerase chain reaction analysis revealed that chronic myocardial ischemia produced a biphasic response in both hypoxic-inducible factor 1 and stromal-derived factor 1 mRNA expression. While initially unregulated, a gradual decline in hypoxic-inducible factor 1 and stromal-derived factor 1 mRNA expression was observed over time (from day 45 to 90). On serial assessment, endothelial progenitor cell migration in response to chemo attractant gradients of vascular endothelial growth factor (10-200 ng/mL) and stromal cell-derived factor-1 (10-100 ng/mL) was progressively impaired. Decreased circulating levels and migratory dysfunction of bone marrow derived endothelial progenitor cells were documented in a reproducible clinically relevant model of myocardial ischemia. Our model of chronic ischemic cardiac dysfunction could contribute to improved understanding of cellular mechanisms involved in the mobilization and exhaustion of endothelial progenitor cells in patients with heart failure.

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