This study by Sedding and colleagues suggests a mechanism for FSAP in vascular biology, in particular the smooth muscle cell-dependent neo-intima formation in atherogenic plaque formation.

Based upon the observation (i) that FSAP is present in atherosclerotic plaques and (ii) that FSAP inhibits vascular smooth muscle cell activation in vitro, they analysed the effect of wild-type (WT)and mutant (M1) FSAP on neo-intima formation in vivo.

In an animal model (“mouse-femoral artery after wire-induced injury”) they found that wild type-FSAP led to a 70 % reduction in neo-intima formation, while FSAP-M1 had no effect. This difference in neo-intima formation was related to a difference between wild-type FSAP and FSAP-MI in cleavage activity towards platelet-derived growth factor (PDGF).

The authors conclude that FSAP has a protective function in the vasculature, and that the MI polymorphism might be clinically relevant in re-stenosis.

Authors and Source:
Sedding et al., J Exp Med, , 2006 Vol. 203, No. 13, December 25: 2801–2807

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