Increased plasma tissue factor levels in acute myocardial infarction

Suefuji, Hisakazu; Ogawa, Hisao; Yasue, Hirofumi; Kaikita, Koichi; Soejima, Hirofumi; Motoyama, Takeshi; Mizuno, Yuji; Oshima, Shuichi; Saito, Taro; Tsuji, Ichiro; Kumeda, Kousuke; Kamikubo, Yu-ichi; Nakamura, Shin

doi:10.1016/s0002-8703(97)70132-7

Cited by 138 publications

(99 citation statements)

References 20 publications

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“…Our findings suggest that the microvesicle TF contributes to a relevant extent to this prothrombotic state. In line with this conclusion, high plasma TF contents have been observed under pathological conditions predisposing for thrombosis (7)(8)(9). Indeed, when present in normal concentrations, the microvesicle TF was found to account already for about one-half of the overall TF-mediated activation of coagulation.…”

Section: Discussionmentioning

confidence: 56%

Intravascular tissue factor initiates coagulation via circulating microvesicles and platelets

Müller¹,

Klocke²,

Alex³

et al. 2003

FASEB j.

364

275

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Although tissue factor (TF), the principial initiator of physiological coagulation and pathological thrombosis, has recently been proposed to be present in human blood, the functional significance and location of the intravascular TF is unknown. In the plasma portion of blood, we found TF to be mainly associated with circulating microvesicles. By cell sorting with the specific marker CD42b, platelet-derived microvesicles were identified as a major location of the plasma TF. This was confirmed by the presence of full-length TF in microvesicles acutely shedded from the activated platelets. TF was observed to be stored in the α-granules and the open canalicular system of resting platelets and to be exposed on the cell surface after platelet activation. Functional competence of the blood-based TF was enabled when the microvesicles and platelets adhered to neutrophils, as mediated by P-selectin and neutrophil counterreceptor (PSGL-1, CD18 integrins) interactions. Moreover, neutrophil-secreted oxygen radical species supported the intravascular TF activity. The pools of platelet and microvesicle TF contributed additively and to a comparable extent to the overall blood TF activity, indicating a substantial participation of the microvesicle TF. Our results introduce a new concept of TF-mediated coagulation crucially dependent on TF associated with microvesicles and activated platelets, which principally enables the entire coagulation system to proceed on a restricted cell surface.Key words: lipopolysaccharide • platelet rich plasma • superoxide dismutase • catalase • microparticles T wo principal events that are initiated after disrupture of the endothelial barrier are thought to mark the initiation of hemostasis. Blood platelets adhere to subendothelial collagen providing a provisional, mechanically unstable closure of the vessel perforation. Concomitantly, the coagulation process is started. This is mainly due to the formation of an initiator complex between tissue factor (TF), an integral cell membrane protein predominantly present in the adventitial layer of the vessel wall, and the blood-based factor VII/VIIa (1). The TF/factor VIIa complex proteolytically activates factor X, which, in turn, elicits the formation of thrombin. The TF/factor VIIa complex is likely to play a central role in the genesis of arterial and venous thrombosis (2, 3), leading causes of mortality in many countries. TF is present in the lipid rich core of unstable atherosclerotic plaques and may be a major determinant of the thrombogenicity of the plaques (4-6). Indeed, on rupture of the plaque, the interaction of TF with factor VIIa substantially contributes to the rapid formation of the occluding thrombus, the principal final step in the genesis of coronary ischemic disease.Apart from its presence in the vascular wall, TF has also been detected in the blood (intravascular TF). So far, no clear conclusion has been reached about the localization and the functional meaning of the blood-based TF. In the plasma compartment, TF is present un...

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Section: Discussionmentioning

confidence: 56%

Intravascular tissue factor initiates coagulation via circulating microvesicles and platelets

Müller¹,

Klocke²,

Alex³

et al. 2003

FASEB j.

364

275

View full text Add to dashboard Cite

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“…Plasma TF concentration has been reported to be increased in various disease such as disseminated intravascular coagulation (DIC), ischaemic heart disease, antiphospholipid syndrome, and cancer (Koyama et al, 1994;Takahashi et al, 1994;Wada et al, 1994;Suefuji et al, 1997;Cuadrando et al, 1998;Falciani et al, 1998;Misumi et al, 1998). We showed that plasma TF concentration was up-regulated in primary and recurrent breast cancer patients.…”

Section: mentioning

confidence: 48%

Tissue factor expression in breast cancer tissues: its correlation with prognosis and plasma concentration

Ueno¹,

Toi²,

et al. 2000

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Tissue factor (TF), an initiator of the extrinsic coagulation cascade, is expressed in a wide range of cancer cells and plays important roles in cancer progression and metastasis. Recently, the intracellular function of TF has been revealed to be involved in cancer invasion, independent of the blood coagulation pathway. To evaluate the clinical significance of TF expression, we performed an enzyme-linked immunosorbent assay (ELISA) in the plasma of 67 breast cancer patients and immunohistochemistry in 213 breast cancer tissues. In the ELISA study, we showed an up-regulation of plasma TF concentration in breast cancer patients compared with normal controls. Immunohistochemistry demonstrated that TF was expressed in tumour cells and stromal cells and tumour TF expression closely correlated with stromal TF expression ( P = 0.0005). The concentration of plasma TF was associated with tissue TF expression in both tumour and stroma. The multivariate analysis demonstrated that tumour TF expression was an independent prognostic indicator for overall survival ( P = 0.0452). Our data show that plasma TF concentration reflects tissue TF expression and tumour TF expression can provide some predictive value for prognosis and distant metastasis, which indicates the importance of TF function in tumour progression. © 2000 Cancer Research Campaign

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“…In this condition the coagulation was mainly dependent on the concentration of endogenous TF, as described previously. 23,24 The effect of heparanase was also tested in whole blood using thromboelastography. Citrated blood samples from healthy donors to which factor VIIa (0.04 μM) and factor X (1.4 μM) were added were recalcified according to the manufacturer's recommendations (final concentration of CaCl2 8 mM) and arranged in the disposable cups of the thromboelastogram.…”

Section: Heparanase In Human Plasmamentioning

confidence: 99%

Heparanase enhances the generation of activated factor X in the presence of tissue factor and activated factor VII

Nadir¹,

Brenner²,

Fux³

et al. 2010

Haematologica

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BackgroundHeparanase is an endo-β-D-glucuronidase dominantly involved in tumor metastasis and angiogenesis. Recently, we demonstrated that heparanase is involved in the regulation of the hemostatic system. Our hypothesis was that heparanase is directly involved in activation of the coagulation cascade. Design and MethodsActivated factor X and thrombin were studied using chromogenic assays, immunoblotting and thromboelastography. Heparanase levels were measured by enzyme-linked immunosorbent assay. A potential direct interaction between tissue factor and heparanase was studied by coimmunoprecipitation and far-western assays. ResultsInterestingly, addition of heparanase to tissue factor and activated factor VII resulted in a 3-to 4-fold increase in activation of the coagulation cascade as shown by increased activated factor X and thrombin production. Culture medium of human embryonic kidney 293 cells overexpressing heparanase and its derivatives increased activated factor X levels in a non-enzymatic manner. When heparanase was added to pooled normal plasma, a 7-to 8-fold increase in activated factor X level was observed. Subsequently, we searched for clinical data supporting this newly identified role of heparanase. Plasma samples from 35 patients with acute leukemia at presentation and 20 healthy donors were studied for heparanase and activated factor X levels. A strong positive correlation was found between plasma heparanase and activated factor X levels (r=0.735, P=0.001). Unfractionated heparin and an inhibitor of activated factor X abolished the effect of heparanase, while tissue factor pathway inhibitor and tissue factor pathway inhibitor-2 only attenuated the procoagulant effect. Using co-immunoprecipitation and farwestern analyses it was shown that heparanase interacts directly with tissue factor. ConclusionsOverall, our results support the notion that heparanase is a potential modulator of blood hemostasis, and suggest a novel mechanism by which heparanase increases the generation of activated factor X in the presence of tissue factor and activated factor VII.Key words: heparanase, coagulation cascade, tissue factor, Xa level.Citation: Nadir Y, Brenner B, Fux L, Shafat I, Attias J, and Vlodavsky I. Heparanase enhances the generation of activated factor X in the presence of tissue factor and activated factor VII. Haematologica 2010;95(11):1927-1934. doi:10.3324/haematol.2010 Heparanase enhances the generation of activated factor X in the presence of tissue factor and activated factor VII

show abstract

Increased plasma tissue factor levels in acute myocardial infarction

Cited by 138 publications

References 20 publications

Intravascular tissue factor initiates coagulation via circulating microvesicles and platelets

Intravascular tissue factor initiates coagulation via circulating microvesicles and platelets

Tissue factor expression in breast cancer tissues: its correlation with prognosis and plasma concentration

Heparanase enhances the generation of activated factor X in the presence of tissue factor and activated factor VII

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