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1 Cardiology, Leiden University Medical Center, Leiden, Netherlands
2 Anatomy and Embryology, Leiden University Medical Center, Leiden, Netherlands
3 Molecular Cell Biology, Leiden University Medical Center, Leiden, Netherlands; Cardiology, Leiden University Medical Center, Leiden, Netherlands
4 Division of Image Processing, Leiden University Medical Center, Leiden, Netherlands
5 Molecular Cell Biology, Leiden University Medical Center, Leiden, Netherlands
* To whom correspondence should be addressed. E-mail: D.E.Atsma{at}lumc.nl.
Objective: Mesenchymal stem cells (MSCs) from healthy donors improve cardiac function in experimental acute myocardial infarction (AMI) models. However, little is known about the therapeutic capacity of human MSCs (hMSCs) from patients with ischemic heart disease (IHD). Therefore, the behavior of hMSCs from IHD patients in an immune-compromised mouse AMI model was studied. Methods: eGFP labeled hMSCs from IHD patients (hMSC group: 2 x 105 cells in 20 µl, n=12) or vehicle only (Medium group: n=14) were injected into infarcted myocardium of NOD/scid mice. Sham-operated mice were used as Control (n=10). Cardiac anatomy and function were serially assessed using 9.4-T magnetic resonance imaging (MRI); 2 weeks after cell transplantation immunohistological analysis was performed. Results: At day 2, delayed-enhancement MRI showed no difference in MI size between the hMSC and Medium groups (33±2% versus 36±2%; p=ns). A comparable increase in left ventricular (LV) volume, and decrease in ejection fraction (EF) was observed in both MI groups. However, at day 14, EF was higher in the hMSC than in the medium group (24±3% versus 16±2%; p<0.05). This was accompanied by increased vascularity and reduced thinning of the infarct scar. Engrafted hMSCs (4.1±0.3% of injected cells) expressed von Willebrand factor (16.9±2.7%) but no stringent cardiac or smooth muscle markers. Conclusions: hMSCs from patients with IHD engraft in infarcted mouse myocardium and preserve LV function, two weeks after acute myocardial infarction, potentially through enhancement of scar vascularity and reduction of wall thinning.
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