Factor VII Activating Protease (FSAP) has been implied in the progression of atherosclerosis, and particularly in coronary artery disease, and the development of associated clinical events.

Along these lines Parahuleva and colleagues examined the relation between plasma concentration of FSAP and pro-inflammatory activation of macrophages and the signalling pathways induced by FSAP.

FSAP treatment induced IkappaB-dependent NF-kappaB activation in freshly isolated human monocytes. FSAP also induced the phosphorylation and proteolytic degradation of the inhibitor IkappaBα. Moreover, the phosphorylation of p65, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, was induced by  FSAP.

Expression of NF-kappaB, ICAM, IL-6, and tissue factor, all of which under the control of NF-kB, was increased by FSAP.

The authors conclude that FSAP may play a novel role in atherosclerosis by enhancing the inflammatory response of human monocytes/macrophages via NF-kappaB activation.

Authors and Source:
M. Parahuleva, R. Maj, A. Staubitz, H. Hoelscherman, H. Tillmanns, A. Erdogan, S. Kanse.
Poster presentation ISTH 2009: OC-WE-128  

Title:
Factor VII activating protease (FSAP) – inflammation and coagulation cross-talk in patients with coronary artery disease