Title: 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
Authors: Feng, Yingmei
van Eck, Miranda
Van Craeyveld, Eline
Jacobs, Frank
Carlier, Vincent
Van Linthout, Sophie
Erdel, Martin
Tjwa, Marc
De Geest, Bart # ×
Issue Date: 15-Jan-2009
Publisher: W.B. Saunders
Series Title: Blood vol:113 issue:3 pages:755-764
Abstract: 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 HDL cholesterol following human apo A-I (AdA-I) transfer requires scavenger receptor (SR)-BI expression in bone marrow-derived EPCs. Following AdA-I transfer, the number of circulating EPCs increased 2.0-fold (p<0.0001) 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 HDL on EPC migration in vitro requires signaling via SR-BI and extracellular signal-regulated kinases (ERK) and is dependent on increased 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<0.001) 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.
ISSN: 0006-4971
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Molecular and Vascular Biology
Vesalius Research Centre (-)
× corresponding author
# (joint) last author

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