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European Heart Journal Advance Access originally published online on November 13, 2008
European Heart Journal 2009 30(3):346-355; doi:10.1093/eurheartj/ehn501
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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

Reduced number and function of endothelial progenitor cells in patients with aortic valve stenosis: a novel concept for valvular endothelial cell repair

Yasuharu Matsumoto1, Volker Adams1,*, Claudia Walther1, Caroline Kleinecke1, Peter Brugger1, Axel Linke1, Thomas Walther2, Friedrich Wilhelm Mohr2 and Gerhard Schuler1

1 Department of Cardiology, Heart Center Leipzig, University of Leipzig, Strümpellstrasse 39, D-04289 Leipzig, Germany
2 Department of Cardiac Surgery, Heart Center Leipzig, University of Leipzig, Strümpellstrasse 39, D-04289 Leipzig, Germany

Received 13 June 2008; revised 27 September 2008; accepted 16 October 2008; online publish-ahead-of-print 13 November 2008.

* Corresponding author. Tel: +49 341 865 1671, Fax: +49 341 865 1461, Email: adav{at}medizin.uni-leipzig.de

Aims: Endothelial destruction and calcification primarily occur at the aortic side of the calcified aortic valves (AVs). This study investigated whether degenerative AV stenosis (AS) is associated with the presence of valvular endothelial senescence and a reduction in the number and function of endothelial progenitor cells (EPCs).

Methods and results: Fifteen patients with severe AS and 18 age-matched control subjects were enrolled. Senescence-associated β-galactosidase activity was mostly localized on the valvular endothelial cells (ECs) of the explanted AVs and highly coincided with the calcified lesion at the aortic side. The number (9.3 ± 8.3 vs. 20.5 ± 9.0 cells per 106 mononuclear cells; P < 0.01) and the migratory capacity (107.8 ± 54.6 vs. 185.0 ± 68.8 cells per 1000 cells; P < 0.01) of EPCs evaluated by FACS analysis or migration assay were significantly reduced in AS when compared with control. As possible mechanisms of alterations in EPCs, caspase-3 activity was significantly increased, whereas telomere-repeating factor-2 expression quantified by western blot was significantly reduced in EPCs from AS when compared with control.

Conclusion: Reduced regenerative capacity of valvular ECs due to senescence and decreased levels of EPCs might be, at least in part, a pathological link for the destruction of valvular ECs, resulting in progression of degenerative AS.

Key Words: Aortic valve stenosis • Apoptosis • Endothelial progenitor cells • Senescence • Ageing


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