Local Irrigation With Tissue Factor Pathway Inhibitor Inhibits Intimal Hyperplasia Induced by Arterial Interventions

Brown, David M.; Kania, Norbert; Choi, Eric T.; Lantieri, Laurent; Pasia, E. Neil; Wun, Tze-Chein; Khouri, Roger K.

doi:10.1001/archsurg.1996.01430220080018

Cited by 25 publications

(17 citation statements)

References 25 publications

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“…It is possible that increased TF expression at injured atherosclerotic coronary lesions enhances thrombin generation in the coronary circulation. Several previous studies demonstrated that inhibition of TF binding to other coagulation factors prevented restenosis of balloon-injured arteries in animal models [31, 32, 33]. Inhibition of initiation of the extrinsic coagulation pathway was suggested to be important in those studies.…”

Section: Discussionmentioning

confidence: 99%

Tissue Factor Expression in Coronary Circulation as a Prognostic Factor for Late Restenosis after Coronary Angioplasty

et al. 2001

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We investigated changes in blood coagulation in the coronary circulation after percutaneous transluminal coronary angioplasty (PTCA) and its clinical significance. We examined 43 patients with ischemic heart disease who underwent elective PTCA of isolated stenotic lesions in the left coronary artery. Ten patients underwent PTCA alone, 15 received percutaneous transluminal rotational atherectomy (PTRA) and 18 stent implantation. Blood samples were drawn from the coronary sinus before and immediately after PTCA, as well as 4 and 24 h later. Plasma levels of tissue factor (TF), thrombin-antithrombin III complex (TAT) and prothrombin fragment 1+2 (F 1+2) were measured by enzyme-linked immunosorbent assay. Follow-up coronary angiography was performed 6 months after PTCA. Minimal luminal diameter was assessed by quantitative coronary angiography to evaluate late loss index. TF, TAT and F 1+2 levels in the coronary sinus blood showed significant increases 24 h after PTCA. A significant positive correlation was found between changes in TF levels 24 h after PTCA and late loss index 6 months after the procedure. TF levels in the coronary sinus blood were significantly higher in patients with late restenosis than in those without restenosis. These results suggest that TF expression in the coronary circulation after PTCA is a prognostic factor for late restenosis.

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Section: Discussionmentioning

confidence: 99%

Tissue Factor Expression in Coronary Circulation as a Prognostic Factor for Late Restenosis after Coronary Angioplasty

et al. 2001

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“…Recombinant TFPI can prevent thrombosis and restenosis after arterial injury in cell culture systems in vitro and in various animal models. [81][82][83][84][85][86][87][88][89][90][91][92] There are also reports that endogenous TFPI is involved in the process of thrombus formation in vivo and that it plays an active role in modulating arterial stenosis. 93 These results indicate that the intravenous administration of recombinant TFPI protein prevents thrombosis at an early stage and restenosis at a later stage.…”

Section: Potential Roles Of Tfpi In Atherogenesismentioning

confidence: 99%

Regulation of Functions of Vascular Wall Cells by Tissue Factor Pathway Inhibitor

Kato

2002

ATVB

143

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Abstract-Tissue factor pathway inhibitor (TFPI) is a Kunitz-type protease inhibitor that inhibits the initial reactions of blood coagulation. A major pool of TFPI is the form associated with the surface of endothelial cells, which is speculated to play an important role in regulating the functions of vascular wall cells. TFPI consists of 3 tandem Kunitz inhibitor domains, the first and second of which inhibit the tissue factor-factor VIIa complex and factor Xa, respectively. Recent findings indicate that TFPI has another function, ie, the modulation of cell proliferation. This function is based on the interaction of the C-terminal region of TFPI with these cells. Key Words: tissue factor pathway inhibitor Ⅲ blood coagulation Ⅲ thrombosis Ⅲ restenosis Ⅲ vascular wall cells B lood coagulation is initiated by the interaction of factor VII in plasma with tissue factor (TF) at the site of blood vessel injury, and the TF-factor VIIa complex activates factor X and factor IX, leading to the generation of thrombin. Vascular wall cells play a central role in the regulation of hemostasis by the cellular control of procoagulant and anticoagulant mechanisms. Normal endothelial cells do not show detectable levels of TF, although expression of endothelial TF occurs in vitro after perturbation with different agonists. On the other hand, increased TF levels have been detected in atherosclerotic plaque, probably reflecting secretion by smooth muscle cells, monocytes/macrophages, and endothelial cells.The TF pathway inhibitor (TFPI) is a Kunitz-type protease inhibitor that inhibits the initial reactions of blood coagulation. A major pool of TFPI is the form associated with the surface of endothelial cells, which is speculated to play an important role in the regulation of the functions of vascular wall cells. Recent findings indicate that TFPI has another function, ie, the modulation of cell proliferation. Many reviews on TFPI have been published. [1][2][3][4][5] The structure and biology of TFPI have recently been reviewed. 6 Recent findings related to regulation of the functions of vascular wall cells by TFPI in physiological and pathological conditions will be summarized in the present review. Functional Domains of TFPIEver since the determination of the amino acid sequence of human TFPI 14 years ago, 7 a number of studies have been published on the structure and functions of TFPI. The amino acid sequences of TFPI from monkeys, rabbits, dogs, rats, and mice have been reported. Many investigators have examined the properties of TFPI by using recombinant proteins. As shown in Figure 1, TFPI mRNA is expressed from the TFPI gene, which consists of 9 exons. Mature TFPI protein consists of 3 tandem Kunitz inhibitor domains, the first and second of which inhibit TF-VIIa and Xa, respectively. The third domain has no inhibitory activity toward proteases. Heparin-binding sites of TFPI are located in the third Kunitz domain and the C-terminal basic region. The inhibitory effect of TFPI on the initiation of blood coagulation and the enhanc...

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“…25 The failure of systemically administered antithrombotic therapy to efficiently interfere with clinical postangioplasty restenosis in humans is thought to be a result of insufficient local concentration of antithrombotic drugs at sites of balloon injury. Thus, various studies with local application strategies of TFPI protein 23,24,[26][27][28][29][30][31] or TFPI gene [32][33][34][35] were undertaken to antagonize local thrombus formation, intimal hyperplasia, or vascular remodeling, generally using a surgical approach for irrigation or transfection. In contrast to these studies, we sought to locally overexpress TFPI using a clinically feasible, catheter-based approach.…”

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confidence: 99%

Inhibition of restenosis by tissue factor pathway inhibitor: in vivo and in vitro evidence for suppressed monocyte chemoattraction and reduced gelatinolytic activity

Kopp

Hölzenbein

Steiner

et al. 2004

Blood

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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.

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Local Irrigation With Tissue Factor Pathway Inhibitor Inhibits Intimal Hyperplasia Induced by Arterial Interventions

Cited by 25 publications

References 25 publications

Tissue Factor Expression in Coronary Circulation as a Prognostic Factor for Late Restenosis after Coronary Angioplasty

Tissue Factor Expression in Coronary Circulation as a Prognostic Factor for Late Restenosis after Coronary Angioplasty

Regulation of Functions of Vascular Wall Cells by Tissue Factor Pathway Inhibitor

Inhibition of restenosis by tissue factor pathway inhibitor: in vivo and in vitro evidence for suppressed monocyte chemoattraction and reduced gelatinolytic activity

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