Pluripotency of tissue resident cells derived from aortic valve leaflets
Objectives: The pathogenesis of cardiac valve degeneration corresponds with the valvular endothelial cells and the emergence of valvular myofibroblasts. In the current study, we identified a population of cells within human aortic valve leaflets that show the properties of both, endothelial cells as...
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Format: | Tagungsbericht |
Sprache: | eng |
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Zusammenfassung: | Objectives:
The pathogenesis of cardiac valve degeneration corresponds with the valvular endothelial cells and the emergence of valvular myofibroblasts. In the current study, we identified a population of cells within human aortic valve leaflets that show the properties of both, endothelial cells as well as. mesenchymal cells.
Material and methods:
Calcific aortic valve (CAV) tissues (n=15) and non-calcific aortic valve (NCAVA) tissues (n=6) were obtained from patients after valve replacement. The expression of markers indicative of endothelial, and mesenchymal progenitor lineages were investigated by immunhistochemical staining. Additionally, valvular cells has been isolated from CAV and NCAV leaflets and characterized by morphological and ultrastructural analysis.
Results:
Our data showed that CAV contained a population of cells within calcific leaflets which stained positive not only for a smooth muscle actin (aSMA) but also for endothelial progenitor markers Tie-2 and vascular endothelial growth factor receptor-2 (VEGFR-2). The pluripotency of cells derived from CAV were shown by the phenotypic difference between cell populations. These cells could differentiate to endothelial as well as mesenchymal cells in vitro. Indeed, ultrastructural analysis showed the heterogenity of cell populations in culture of CAV-derived cells in contrast to cells isolated NCAV.
Conclusion:
The coexpression of Tie-2 and VEGFR-2 as two embryonic vascular progenitor markers with a-SMA suggests a endothelial-mesenchymal origin for the cells involved in valvular degeneration. These cells may be considered as the target for medical therapy and open a new debate in prevention and treatment of this progressive dieses at early stages. |
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ISSN: | 0171-6425 1439-1902 |
DOI: | 10.1055/s-2006-925673 |