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Blood, 15 January 2009, Vol. 113, No. 3, pp. 755-764. Prepublished online as a Blood First Edition Paper on September 29, 2008; DOI 10.1182/blood-2008-06-161794. This Article Full Text Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2008-06-161794v1 113/3/755    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Feng, Y. Articles by De Geest, B. Search for Related Content PubMed PubMed Citation Articles by Feng, Y. Articles by De Geest, B. Related Collections Transplantation Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents VASCULAR BIOLOGY Critical role of scavenger receptor-BI–expressing bone marrow–derived endothelial progenitor cells in the attenuation of allograft vasculopathy after human apo A-I transfer Yingmei Feng1, Miranda van Eck2, Eline Van Craeyveld1, Frank Jacobs1, Vincent Carlier1, Sophie Van Linthout3, Martin Erdel4, Marc Tjwa5, and Bart De Geest1 1 Center for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium; 2 Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Gorlaeus Laboratories, Leiden University, Leiden, The Netherlands; 3 Department of Cardiology, Charité University-Medicine Berlin, Berlin, Germany; 4 Division of Clinical Genetics, Medical University of Innsbruck, Innsbruck, Austria; and 5 Vesalius Research Center, Flanders Institute for Biotechnology (VIB), University of Leuven, Leuven, Belgium and Leibniz AG, Center for Molecular Medicine, Institute of Cardiovascular Regeneration, University of Frankfurt, Frankfurt, Germany Allograft vasculopathy is the leading cause of death in patients with heart transplantation. Accelerated endothelial regeneration mediated by enhanced endothelial progenitor cell (EPC) incorporation may attenuate the development of allograft vasculopathy. We investigated the hypothesis that modulation of EPC biology and attenuation of allograft vasculopathy by increased high-density lipoprotein cholesterol after human apo A-I (AdA-I) transfer requires scavenger receptor (SR)–BI expression in bone marrow–derived EPCs. After AdA-I transfer, the number of circulating EPCs increased 2.0-fold (P < .001) at different time points in C57BL/6 mice transplanted with SR-BI+/+ bone marrow but remained unaltered in mice with SR-BI–/– bone marrow. The effect of high-density lipoprotein on EPC migration in vitro requires signaling via SR-BI and extracellular signal-regulated kinases and is dependent on increased nitric oxide (NO) production in EPCs. Human apo A-I transfer 2 weeks before paratopic artery transplantation reduced intimal area at day 21 3.7-fold (P < .001) in mice with SR-BI+/+ bone marrow but had no effect in mice with SR-BI–/– bone marrow. AdA-I transfer potently stimulated EPC incorporation and accelerated endothelial regeneration in chimeric SR-BI+/+ mice but not in chimeric SR-BI–/– mice. In conclusion, human apo A-I transfer accelerates endothelial regeneration mediated via SR-BI expressing bone marrow–derived EPCs, thereby preventing allograft vasculopathy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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