The Journal of Experimental Medicine
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Published online December 4, 2006
doi:10.1084/jem.20052546
The Journal of Experimental Medicine, Vol. 203, No. 13, 2801-2807
The Rockefeller University Press, 0022-1007 $30.00
© 2006 Sedding et al.
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BRIEF DEFINITIVE REPORT

 The G534E polymorphism of the gene encoding the factor VII–activating protease is associated with cardiovascular risk due to increased neointima formation

Daniel Sedding1,2, Jan-Marcus Daniel1, Lars Muhl1, Karin Hersemeyer1, Hannes Brunsch2, Bettina Kemkes-Matthes2, Ruediger C. Braun-Dullaeus3, Harald Tillmanns2, Thomas Weimer4, Klaus T. Preissner1, and Sandip M. Kanse1

1 Institute for Biochemistry and 2 Internal Medicine I/Cardiology, Justus-Liebig-University, 35392 Giessen, Germany
3 Internal Medicine II/Cardiology, Dresden Technology University, 01307 Dresden, Germany
4 ZLB Behring, 35002 Marburg, Germany

CORRESPONDENCE Sandip M. Kanse: sandip.kanse{at}biochemie.med.uni-giessen.de

The G534E polymorphism (Marburg I [MI]) of factor VII–activating protease (FSAP) is associated with carotid stenosis and cardiovascular disease. We have previously demonstrated that FSAP is present in atherosclerotic plaques and it is a potent inhibitor of vascular smooth muscle proliferation and migration in vitro. The effect of wild-type (WT)- and MI-FSAP on neointima formation in the mouse femoral artery after wire-induced injury was investigated. Local application of WT-FSAP led to a 70% reduction in the neointima formation, and this effect was dependent on the protease activity of FSAP. MI-FSAP did not inhibit neointima formation in vivo. This is due to a reduced proteolytic activity of MI-FSAP, compared to WT-FSAP, toward platelet-derived growth factor BB, a key mediator of neointima development. The inability of MI-FSAP to inhibit vascular smooth muscle accumulation explains the observed linkage between the MI-polymorphism and increased cardiovascular risk. Hence, FSAP has a protective function in the vasculature, and analysis of MI polymorphism is likely to be clinically relevant in restenosis.


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