The Journal of Experimental Medicine
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Published online 4 December 2006. doi:10.1084/jem.20052546
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© The Rockefeller University Press, 0022-1007
The Journal of Experimental Medicine

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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