Copyright © 2004 by the European Society of Cardiology.
Clinical research
Cellular repopulation of myocardial infarction in patients with sex-mismatched heart transplantation
a Department of Cardiology and Pneumology, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
b Department of Haematology/Oncology, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
c Division of Pathology, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
d Division of Cytopathology, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
e Heart- and Diabetes-Centre NRW, Bad Oeynhausen, Germany
f Department of Pathology, Central Hospital Bielefeld, Germany
Received August 13, 2003;
revised January 12, 2004;
accepted January 22, 2004
* Corresponding author. Tel.: +49-551-3912667; fax: +49-551-392953
E-mail address: elisabeth.hoecht{at}med.uni-goettingen.de
Aims Recent studies have suggested that human extracardiac progenitor cells are capable of differentiating into cardiomyocytes. In animal studies, myocardial infarction attracted bone marrow stem cells and enhanced their differentiation into cardiomyocytes. Based on these findings, we hypothesised that myocardial infarction stimulates the invasion of progenitor cells and their differentiation into endothelial and cardiac cells in the human heart.
Methods and results We compared autopsy samples from male control patients who had received a female donor heart with samples from such patients who developed myocardial infarction after transplantation. Fluorescence in situ hybridisation (FISH) for detection of the Y-chromosome was combined with immunofluorescence staining for CD45 and CD68 to distinguish host-derived inflammatory cells. Additionally, we used a 3D-confocal imaging technique to indisputably assign Y-chromosome-positive nuclei to their cytoplasm. In patients with myocardial infarction after heart transplantation (
), host-derived non-inflammatory progenitor and endothelial cells were significantly increased compared to non-infarcted patients (
). Yet, by using this novel multi-step approach, only 0.02% of all cells were estimated to be male cardiomyocytes and their increase in infarcted regions to 0.07% was not significant.
Conclusion Myocardial infarction enhances the invasion of extracardiac progenitor cells and their regeneration of endothelial cells. However, a significant differentiation into cardiomyocytes as a physiological mechanism of postischaemic regeneration does not occur in transplanted patients.
Key Words: Stem cells • Myocardial infarction • Chimerism • Cardiac regeneration • Three-dimensional confocal microscopy
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