Abstract:
:Activation of inflammatory and procoagulant mechanisms is thought to contribute significantly to the initiation of restenosis, a common complication after balloon angioplasty of obstructed arteries. During this process, expression of tissue factor (TF) represents one of the major physiologic triggers of coagulation that results in thrombus formation and the generation of additional signals leading to vascular smooth muscle cell (VSMC) proliferation and migration. In this study, we have investigated the mechanisms by which inhibition of coagulation at an early stage through overexpression of tissue factor pathway inhibitor (TFPI), an endogenous inhibitor of TF, might reduce restenosis. In a rabbit femoral artery model, percutaneous delivery of TFPI using a recombinant adenoviral vector resulted in a significant reduction of the intimamedia ratio 21 days after injury. Investigating several markers of inflammation and coagulation, we found reduced neointimal expression of monocyte chemoattractant protein-1 (MCP-1), lesional monocyte infiltration, and expression of vascular TF, matrix metalloproteinase-2 (MMP-2), and MMP-9. Moreover, overexpression of TFPI suppressed the autocrine release of platelet-derived growth factor BB (PDGF-BB), MCP-1, and MMP-2 in response to factors VIIa and Xa from VSMCs in vitro and inhibited monocyte TF activity. These results suggest that TFPI exerts its action in vivo through not only thrombotic, but also nonthrombotic mechanisms.
journal_name
Bloodjournal_title
Bloodauthors
Kopp CW,Hölzenbein T,Steiner S,Marculescu R,Bergmeister H,Seidinger D,Mosberger I,Kaun C,Cejna M,Horvat R,Wojta J,Maurer G,Binder BR,Breuss JM,Ecker RC,de Martin R,Minar Edoi
10.1182/blood-2003-04-1148subject
Has Abstractpub_date
2004-03-01 00:00:00pages
1653-61issue
5eissn
0006-4971issn
1528-0020pii
2003-04-1148journal_volume
103pub_type
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