Expression of Functional Tissue Factor on Small Vesicles of Lipopolysaccharide- Stimulated Human Vascular Endothelial Cells

Kagawa, Hideo; Komiyama, Yutaka; Nakamura, Shin; Miyake, Tetsuya; Miyazaki, Yasuhiko; Hamamoto, Kenjirou; Masuda, Midori; Takahashi, Hakuo; Nomura, Shosaku; Fukuhara, Shirou

doi:10.1016/s0049-3848(98)00108-x

Cited by 67 publications

(51 citation statements)

References 27 publications

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“…In vitro, platelets are known to release microparticles that expose PS and bind coagulation factors V, VIII, IX, and XI and/or their activated forms (5)(6)(7)(8). Monocytes, endothelial cells, and erythrocytes also release PS-exposing microparticles upon appropriate activation, which supports coagulation in vitro (9)(10)(11). In vivo, microparticles can be found in the systemic circulation; their numbers and cellular origin are dependent on the state of health of the individual.…”

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confidence: 75%

Cell‐derived microparticles in synovial fluid from inflamed arthritic joints support coagulation exclusively via a factor VII–dependent mechanism

Berckmans¹,

Nieuwland²,

Tak³

et al. 2002

Arthritis & Rheumatism

180

169

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Objective. To determine the cellular origin of synovial microparticles, their procoagulant properties, and their relationship to local hypercoagulation.Methods. Microparticles in synovial fluid and plasma from patients with rheumatoid arthritis (RA; n ‫؍‬ 10) and patients with other forms of arthritis (non-RA; n ‫؍‬ 10) and in plasma from healthy subjects (n ‫؍‬ 20) were isolated by centrifugation. Microparticles were identified by flow cytometry. The ability of microparticles to support coagulation was determined in normal plasma. Concentrations of prothrombin fragment F 1؉2 (by enzyme-linked immunosorbent assay [ELISA]) and thrombin-antithrombin (TAT) complexes (by ELISA) were determined as estimates of the coagulation activation status in vivo.Results. Plasma from patients and healthy controls contained comparable numbers of microparticles, which originated from platelets and erythrocytes. Synovial microparticles from RA patients and non-RA patients originated mainly from monocytes and granulocytes; few originated from platelets and erythrocytes. Synovial microparticles bound less annexin V (which binds to negatively charged phospholipids) than did plasma microparticles, exposed tissue factor, and supported thrombin generation via factor VII. F 1؉2 (median 66 nM) and TAT complex (median 710 g/liter) concentrations were elevated in synovial fluid compared with plasma from the patients (1.6 nM and 7.0 g/liter, respectively) as well as the controls (1.0 nM and 2.9 g/liter, respectively). Conclusion. Synovial fluid contains high numbers of microparticles derived from leukocytes that are strongly coagulant via the factor VII-dependent pathway. We propose that these microparticles contribute to the local hypercoagulation and fibrin deposition in inflamed joints of patients with RA and other arthritic disorders.

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mentioning

confidence: 75%

Cell‐derived microparticles in synovial fluid from inflamed arthritic joints support coagulation exclusively via a factor VII–dependent mechanism

Berckmans¹,

Nieuwland²,

Tak³

et al. 2002

Arthritis & Rheumatism

180

169

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“…42 Indeed, the presence of small vesicles containing TF in the medium of stimulated endothelial cells has recently been described. 44 As previously mentioned, caveolaeassociated TF has also been proposed to contribute to endothelial regulation of hemostasis, owing to its colocalization with thrombomodulin and urokinase receptor. 42 The expression of TF is thought to be responsible for the thrombotic complications associated with septic shock, cancer, and atherosclerosis.…”

Section: Discussionmentioning

confidence: 97%

Cooperation Between VEGF and TNF-α Is Necessary for Exposure of Active Tissue Factor on the Surface of Human Endothelial Cells

Camera

Giesen

Fallon³

et al. 1999

ATVB

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Abstract-This study was undertaken to characterize tissue factor (TF) induction, localization, and functional activity in cultured human umbilical vein endothelial cells (HUVECs) exposed to recombinant vascular endothelial growth factor (rVEGF) and recombinant tumor necrosis factor-␣ (rTNF-␣). rVEGF (1 nmol/L) and rTNF-␣ (500 U/mL) synergistically increased TF mRNA, protein, and total activity, as measured in cell lysates. To examine surface TF expression, living cells were treated with antibody to TF and examined microscopically. Almost no staining was seen in control cells or cells treated with a single agent. In contrast, cells treated with both agonists showed intense membrane staining with surface patches, appearing as buds by confocal microscopy. To determine surface TF activity, studies were performed using a parallel-plate flow chamber, which allows detection of factor Xa generation on living cells. rVEGF and rTNF-␣ induced little surface TF activity (0.032Ϯ0.008 and 0.014Ϯ0.008 fmol/cm 2 , respectively). In combination, they significantly increased TF expression on the cell surface (0.429Ϯ0.094 fmol/cm 2 , PϽ0.05). These data indicate that the synergistic effect of rVEGF and rTNF-␣ is necessary to generate functional TF on the surface of endothelial cells. The requirement for multiple agonists to expose active TF may serve to protect endothelial cells from acting as a procoagulant surface, even under conditions of cell perturbation. (Arterioscler Thromb Vasc Biol. 1999;19:531-537.)

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“…The membrane form of TF is probably shed as a small vesicle that is generated from the cell surface of TF-expressing live cells. 17 Other cases will be cellular fragmentation occurred during apoptosis or necrosis of dying TF-expressing cells. We reported that there is a good correlation between procoagulant activity and plasma membrane-bound TF levels in patients without renal dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Heightened Tissue Factor Associated With Tissue Factor Pathway Inhibitor and Prognosis in Patients With Unstable Angina

et al. 1999

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Background-This study was designed to evaluate the plasma levels of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in patients with unstable angina and investigate whether there is a relationship between these levels and unfavorable outcome. Methods and Results-The plasma TF and free TFPI antigen levels were determined in plasma samples taken from 51 patients with unstable angina, 56 with stable exertional angina, and 55 with chest pain syndrome. The plasma TF and free TFPI antigen levels were higher in the unstable angina group than in the stable exertional angina and chest pain syndrome group. There was a good correlation between TF and TFPI. We established borderline as maximum level in the patients with chest pain syndrome. Seven patients (of the 22 in the high TF group) required revascularization to control their unstable angina during in-hospital stay. On the other hand, only 1 of the 29 patients in the low TF group required myocardial revascularization. Four patients of the 14 patients in the high free TFPI group required myocardial revascularization during in-hospital stay, and 4 of the 37 patients in the low free TFPI group required myocardial revascularization. We compared the TF and free TFPI levels between the cardiac event (ϩ) group and cardiac event (Ϫ) group. TF levels were significantly higher in the cardiac event (ϩ) group than in the cardiac event (Ϫ) group. Conclusions-We have demonstrated that not only the plasma TF levels but also the plasma-free TFPI levels are elevated in patients with unstable angina. Patients with unstable angina and heightened TF and free TFPI are at increased risk for unfavorable outcomes. The heightened TF level was a more important predictor in patients with unstable angina.

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Expression of Functional Tissue Factor on Small Vesicles of Lipopolysaccharide- Stimulated Human Vascular Endothelial Cells

Cited by 67 publications

References 27 publications

Cell‐derived microparticles in synovial fluid from inflamed arthritic joints support coagulation exclusively via a factor VII–dependent mechanism

Cell‐derived microparticles in synovial fluid from inflamed arthritic joints support coagulation exclusively via a factor VII–dependent mechanism

Cooperation Between VEGF and TNF-α Is Necessary for Exposure of Active Tissue Factor on the Surface of Human Endothelial Cells

Heightened Tissue Factor Associated With Tissue Factor Pathway Inhibitor and Prognosis in Patients With Unstable Angina

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