Thromboplastin content in the vessel walls of different arteries and organs of rabbits

Østerud, Bjarne; Tindall, A. R.; Brox, Jan; Olsen, Jan Ole

doi:10.1016/0049-3848(86)90261-6

Cited by 17 publications

(13 citation statements)

References 14 publications

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“…We also failed to find any TF exposure in ECs from rabbits subjected to Schwartzman reaction by the intravenous injection at the 24-hour interval of two doses of LPS. 36 Corroborative evidence was found in two more recent studies on rabbits and rats, in which dual immunohistochemical staining for TF and von Willebrand factor revealed no detectable endothelial TF antigen in the rabbits, 37 and TF mRNA was found in the mononuclear cells but not in the ECs around the hepatic vein of rats subjected to LPS treatment. In apparent contradiction to the latter three studies, one study claimed an increase in procoagulant activity (PCA) identified as TF in thoracic aorta harvested from rabbits subjected to endotoxin injection.…”

Section: Tf In the Endotheliummentioning

confidence: 85%

Sources of Tissue Factor

Østerud

Bjørklid

2006

Semin Thromb Hemost

224

179

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Tissue factor (TF) exhibits a distinct nonuniform tissue distribution. Thus, high levels are found in highly vascularized organs such as the lung, brain, and placenta; intermediate levels in the heart, kidney, intestine, testes, and uterus; and low levels in the spleen, thymus, and liver. Several cell types are known to express TF constitutively, such as astrocytes in the brain, epithelial cells enveloping organs and body surfaces, adventitial fibroblasts and pericytes, and cardial myocytes in the heart. Smooth muscle cells in the media of the vessel wall and monocytes/macrophages contain small amounts of TF, which is enhanced substantially upon activation of the cells. Endothelial cells probably do not express TF. The popular concept of TF serving predominantly as a hemostatic envelope encapsulating the vascular bed has been challenged recently by the observation that blood of healthy individuals may form TF-induced thrombi under conditions entailing shear stress and activated platelets, corroborating the notion of blood-borne TF. Accordingly, small amounts of decrypted TF activity is detected in calcium ionophore-stimulated monocytes, and microparticles from plasma of healthy subjects possess TF-like activity subject to partial inactivation by anti-TF antibody. In addition to microparticles, plasma TF also comprises the soluble alternatively spliced human TF and truncated TF, both of which probably require factor VIIa to be physiologically active. Although it has been suggested that activated platelets possess active TF, the notion of TF as an integral platelet component is contested by more recent data. Rather, platelets may be very important in decrypting monocyte TF activity in a process entailing transfer of TF to activated platelets.

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Section: Tf In the Endotheliummentioning

confidence: 85%

Sources of Tissue Factor

Østerud

Bjørklid

2006

Semin Thromb Hemost

224

179

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“…Histological analysis of human tissues using antibodies [6–8] or labeled FVIIa [1,2] revealed that under normal conditions TF‐bearing cells are physically separated from blood but they ‘envelope’ the circulatory system. TF is absent on the surface of undisturbed endothelial cells, which form the inner lining of blood vessels, and its concentration increases from smooth muscle cells in the media to fibroblasts in the adventitia [3,6,8]. The highest levels of TF are constitutively expressed by cardiac myocytes, lung fibroblasts, cells within the brain and the placenta, i.e.…”

Section: Introductionmentioning

confidence: 99%

“…The highest levels of TF are constitutively expressed by cardiac myocytes, lung fibroblasts, cells within the brain and the placenta, i.e. at sites where protection against hemorrhage after tissue injury is critical [3,6,8]. Under pathological conditions the high level of TF expression by activated vascular cells [endothelial cells (ECs), smooth muscle cells (SMCs), macrophages (MPs)] determines the thrombogenicity of atherosclerotic plaques [2,9] and malignant tumors [1,10] and ultimately leads to intravascular fibrin deposition and thrombus formation.…”

Section: Introductionmentioning

confidence: 99%

Initiation and propagation of coagulation from tissue factor‐bearing cell monolayers to plasma: initiator cells do not regulate spatial growth rate

Ovanesov

Ananyeva

Panteleev

et al. 2005

Journal of Thrombosis and Haemostasis

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To cite this article: Ovanesov MV, Ananyeva NM, Panteleev MA, Ataullakhanov FI, Saenko EL. Initiation and propagation of coagulation from tissue factor-bearing cell monolayers to plasma: initiator cells do not regulate spatial growth rate. J Thromb Haemost 2005; 3: 321-31.Summary. Exposure of tissue factor (TF)-bearing cells to blood is the initial event in coagulation and intravascular thrombus formation. However, the mechanisms which determine thrombus growth remain poorly understood. To explore whether the procoagulant activity of vessel wall-bound cells regulates thrombus expansion, we studied in vitro spatial clot growth initiated by cultured human cells of different types in contact pathway-inhibited, non-flowing human plasma. Human aortic endothelial cells, smooth muscle cells, macrophages and lung fibroblasts differed in their ability to support thrombin generation in microplate assay with peaks of generated thrombin of 60 ± 53 nmol L , 218 ± 55 nmol L )1 and 407 ± 59 nmol L )1 (mean ± SD), respectively. Real-time videomicroscopy revealed the initiation and spatial growth phases of clot formation. Different procoagulant activity of cell monolayers was manifested as up to 4-fold difference in the lag times of clot formation. In contrast, the clot growth rate, which characterized propagation of clotting from the cell surface to plasma, was largely independent of cell type (£ 30% difference). Experiments with factor VII (FVII)-, FVIII-, FX-or FXI-deficient plasmas and annexin V revealed that (i) cell surface-associated extrinsic Xase was critical for initiation of clotting; (ii) intrinsic Xase regulated only the growth phase; and (iii) the contribution of plasma phospholipid surfaces in the growth phase was predominant. We conclude that the role of TF-bearing initiator cells is limited to the initial stage of clot formation. The functioning of intrinsic Xase in plasma provides the primary mechanism of sustained and far-ranging propagation of coagulation leading to the physical expansion of a fibrin clot.

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“…Another intriguing finding in this work is that recombinant activated protein C inhibits TF Ag and procoagulant activity in LPS-activated blood monocytes. In vitro studies have demonstrated that the procoagulant potential of various cells is mediated by the concentration of cell surface TF (61)(62)(63). Thus, the decrease in monocyte cell surface TF Ag and procoagulant activity we report here is likely physiologically important.…”

Section: Figurementioning

confidence: 99%

Activated Protein C Up-Regulates IL-10 and Inhibits Tissue Factor in Blood Monocytes

Toltl¹,

Beaudin

Liaw

2008

The Journal of Immunology

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The protective effect of recombinant activated protein C therapy in patients with severe sepsis likely reflects the ability of recombinant activated protein C to modulate multiple pathways implicated in sepsis pathophysiology. In this study, we examined the effects of recombinant activated protein C on the anti-inflammatory cytokine IL-10 and on the procoagulant molecule tissue factor (TF) in LPS-challenged blood monocytes. Treatment of LPS-stimulated monocytes with recombinant activated protein C resulted in an up-regulation of IL-10 protein production and mRNA synthesis. The up-regulation of IL-10 required the serine protease activity of recombinant activated protein C and was dependent on protease-activated receptor-1, but was independent of the endothelial protein C receptor. At the intracellular level, p38 MAPK activation was required for recombinant activated protein C-mediated up-regulation of IL-10. We further observed that incubation of LPS-stimulated monocytes with recombinant activated protein C down-regulated TF Ag and activity levels. This anticoagulant effect of recombinant activated protein C was dependent on IL-10 since neutralization of endogenously produced IL-10 abrogated the effect. In patients with severe sepsis, plasma IL-10 levels were markedly higher in those treated with recombinant activated protein C than in those who did not receive recombinant activated protein C. This study reveals novel regulatory functions of recombinant activated protein C, specifically the up-regulation of IL-10 and the inhibition of TF activity in monocytes. Our data further suggest that these activities of recombinant activated protein C are directly linked: the recombinant activated protein C-mediated up-regulation of IL-10 reduces TF in circulating monocytes.

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Thromboplastin content in the vessel walls of different arteries and organs of rabbits

Cited by 17 publications

References 14 publications

Sources of Tissue Factor

Sources of Tissue Factor

Initiation and propagation of coagulation from tissue factor‐bearing cell monolayers to plasma: initiator cells do not regulate spatial growth rate

Activated Protein C Up-Regulates IL-10 and Inhibits Tissue Factor in Blood Monocytes

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