Shedding of active tissue factor by aortic smooth muscle cells (SMCs) undergoing apoptosis

被引：23

作者：

Brisset, AC ^{[1
]}

Terrisse, AD ^{[1
]}

Dupouy, D ^{[1
]}

Tellier, L ^{[1
]}

Pech, S ^{[1
]}

Navarro, C ^{[1
]}

Sié, P ^{[1
]}

机构：

[1] Univ Toulouse 3, Lab Rech Hemostase & Thrombose EA 2049, F-31062 Toulouse, France

来源：

THROMBOSIS AND HAEMOSTASIS | 2003年 / 90卷 / 03期

关键词：

apoptosis; arterial thrombosis; smooth muscle cells; tissue factor;

D O I：

10.1160/TH02-12-0291

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

As apoptosis of neo-intimal SMCs is a feature of advanced atherosclerotic plaques, the procoagulant properties of SMCs of synthetic phenotype undergoing apoptosis were investigated. SMCs isolated from rat aorta obtained 10 days after balloon injury, previously found to up-regulate Tissue Factor (TF) and Tissue Factor Inhibitor (TFPI) and to release large amounts of TFPI (Ghrib et aL Thromb Hoemost 2002;87:1043-50), were sensitive to the apoptosis induced by Fas-ligand. During this process, surface TF activity rose by a factor 10 over 6 hours, in parallel with a proportional increase in prothrombinase, while TF protein expressed at the membrane significantly decreased. The microparticles (MPs) produced during SMC death bore intact and functional TF, but the release of TFPI did not change, so that the balance shifted to a procoagulant state during apoptosis. Shed MPs enhanced thrombus formation in flowing whole blood over collagen coated-glass slides. Apoptotic SMCs in atherosclerotic plaques represent a reservoir of highly thrombogenic material, released into the blood stream in case of spontaneous or mechanical plaque disruption.

引用

页码：511 / 518

页数：8

共 26 条

[1]

BOCHATONPIALLAT ML, 1995, AM J PATHOL, V146, P1059

[2] Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque [J].

Bonderman, D ;

Teml, A ;

Jakowitsch, J ;

Adlbrecht, C ;

Gyöngyösi, M ;

Sperker, W ;

Lass, H ;

Mosgoeller, W ;

Glogar, DH ;

Probst, P ;

Maurer, G ;

Nemerson, Y ;

Lang, IM .

BLOOD, 2002, 99 (08) :2794-2800

[3] Human blood-derived macrophages induce apoptosis in human plaque-derived vascular smooth muscle cells by Fass-ligand/Fas interactions [J].

Boyle, JJ ;

Bowyer, DE ;

Weissberg, PL ;

Bennett, MR .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (09) :1402-1407

[4]

BROZE GJ, 1995, THROMB HAEMOSTASIS, V74, P90

[5] Early potent antithrombotic effect with combined aspirin and a loading dose of clopidogrel on experimental arterial thrombogenesis in humans [J].

Cadroy, Y ;

Bossavy, JP ;

Thalamas, C ;

Sagnard, L ;

Sakariassen, K ;

Boneu, B .

CIRCULATION, 2000, 101 (24) :2823-2828

[6] Presence of tissue factor pathway inhibitor in human atherosclerotic plaques is associated with reduced tissue factor activity [J].

Caplice, NM ;

Mueske, CS ;

Kleppe, LS ;

Simari, RD .

CIRCULATION, 1998, 98 (11) :1051-1057

[7] Expression, localization, and activity of tissue factor pathway inhibitor in normal and atherosclerotic human vessels [J].

Crawley, J ;

Lupu, F ;

Westmuckett, AD ;

Severs, NJ ;

Kakkar, VV ;

Lupu, C .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (05) :1362-1373

[8]

Freyssinet JM, 1999, THROMB HAEMOSTASIS, V82, P727

[9] Fas is expressed in human atherosclerotic intima and promotes apoptosis of cytokine-primed human vascular smooth muscle cells [J].

Geng, YJ ;

Henderson, LE ;

Levesque, EB ;

Muszynski, M ;

Libby, P .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) :2200-2208

[10] The expression of tissue factor and tissue factor pathway inhibitor in aortic smooth muscle cells is up-regulated in synthetic compared to contractile phenotype [J].

Ghrib, F ;

Brisset, AC ;

Dupouy, D ;

Terrisse, AD ;

Navarro, C ;

Cadroy, Y ;

Boneu, B ;

Sié, P .

THROMBOSIS AND HAEMOSTASIS, 2002, 87 (06) :1051-1056

← 1 2 3 →