scholarly journals Consecutive enzyme cascades: complement activation at the cell surface triggers increased tissue factor activity

Blood ◽  
1990 ◽  
Vol 76 (2) ◽  
pp. 361-367 ◽  
Author(s):  
SD Carson ◽  
DR Johnson
Keyword(s):  
Cell Surface ◽  
Tissue Factor ◽  
Complement Activation ◽  
Cell Damage ◽  
Membrane Attack Complex ◽  
Fibrin Clot ◽  
Coagulation Cascade ◽  
Factor Activity ◽  
Physical Damage ◽  
Tissue Factor Activity

Abstract Complement activation at the cell surface initiates cell damage through a series of reactions occurring at the cell membrane and, after assembly of the terminal membrane attack complex, produces leakage of cytoplasmic contents from the cell. It has been documented that chemical or physical damage to cell membranes can cause a rapid increase in the expression of tissue factor procoagulant activity. In this study, antibody-mediated complement activation at the cell surface resulted in increased tissue factor activity, which correlated with cytolysis, as measured by 51-chromium release. Therefore, complement fixation on the cell surface can have a direct and immediate stimulatory effect on the coagulation cascade at the point of its initiation, with formation of a fibrin clot requiring only three consecutive proteolytic reactions after immunologically mediated cell damage.

scholarly journals Consecutive enzyme cascades: complement activation at the cell surface triggers increased tissue factor activity

Blood ◽  
1990 ◽  
Vol 76 (2) ◽  
pp. 361-367
Author(s):  
SD Carson ◽  
DR Johnson
Keyword(s):  
Cell Surface ◽  
Tissue Factor ◽  
Complement Activation ◽  
Cell Damage ◽  
Membrane Attack Complex ◽  
Fibrin Clot ◽  
Coagulation Cascade ◽  
Factor Activity ◽  
Physical Damage ◽  
Tissue Factor Activity

Complement activation at the cell surface initiates cell damage through a series of reactions occurring at the cell membrane and, after assembly of the terminal membrane attack complex, produces leakage of cytoplasmic contents from the cell. It has been documented that chemical or physical damage to cell membranes can cause a rapid increase in the expression of tissue factor procoagulant activity. In this study, antibody-mediated complement activation at the cell surface resulted in increased tissue factor activity, which correlated with cytolysis, as measured by 51-chromium release. Therefore, complement fixation on the cell surface can have a direct and immediate stimulatory effect on the coagulation cascade at the point of its initiation, with formation of a fibrin clot requiring only three consecutive proteolytic reactions after immunologically mediated cell damage.

scholarly journals Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells

2009 ◽  
Vol 7 (1) ◽  
pp. 121-131 ◽  
Author(s):  
H. KOTHARI ◽  
G. KAUR ◽  
S. SAHOO ◽  
S. IDELL ◽  
L. V. M. RAO ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Tissue Factor ◽  
Factor Activity ◽  
Tissue Factor Activity

scholarly journals Human Atheromatous Plaque Extracts Induce Tissue Factor Activity (TFa) in Monocytes and also Express Constitutive TFa

1999 ◽  
Vol 81 (01) ◽  
pp. 146-150 ◽  
Author(s):  
Victoria Teodorescu ◽  
Jacob Rand ◽  
Alan Rosman ◽  
Julian Niemetz ◽  
Thomas Muhlfelder
Keyword(s):  
Tissue Factor ◽  
Coagulation Cascade ◽  
Rabbit Brain ◽  
Atheromatous Plaque ◽  
Constitutive Activity ◽  
Factor Activity ◽  
Tissue Factor Activity ◽  
Full Strength ◽  
Very High

SummaryTissue factor activity (TFa) is a major activator of the coagulation cascade and may play a role in atheroma-induced thrombosis. Mono-cyte-macrophages (MO-MF) generate considerable quantities of TFa when stimulated by a variety of inducers. To test the hypothesis that MO could be induced by atheromatous plaque to generate TFa, plaque extracts obtained from patients with obstructive atheromatous disease were used. These extracts were also assayed for constitutive TFa. The constitutive activity was variable from extract to extract but could be very high, up to 250 U TFa. The TFa induced in MO could be also very high, up to 200 U (i.e. 1/5 of the TFa of full strength rabbit brain thromboplastin). These findings point to a major role for MO-MF TFa in the induction or thrombosis by atheromatous plaque.

scholarly journals Complement-mediated regulation of tissue factor activity in endothelium.

1995 ◽  
Vol 182 (6) ◽  
pp. 1807-1814 ◽  
Author(s):  
S Saadi ◽  
R A Holzknecht ◽  
C P Patte ◽  
D M Stern ◽  
J L Platt
Keyword(s):  
Tissue Factor ◽  
Messenger Rna ◽  
Factor Viia ◽  
Interleukin 1 ◽  
Membrane Attack Complex ◽  
Secondary Response ◽  
Cell Surface Expression ◽  
Intermediate Step ◽  
Factor Activity ◽  
Tissue Factor Activity

Inflammation and immunity may be associated with endothelial cell (EC) injury and thrombus formation. We explored the mechanisms through which a humoral immune response directed against the endothelium might promote coagulation. Using the interaction of anti-EC antibodies and complement (C) with cultured EC as a model, we studied the expression and function of tissue factor, a cofactor for factor VIIa-mediated conversion of factor X to Xa. Exposure of EC to anti-EC antibodies and C in sublytic amounts stimulated the synthesis of tissue factor over a period of 16-42 h. Cell surface expression of tissue factor activity required activation of C and assembly of the membrane attack complex, because expression was inhibited by soluble CR1 and was not detected in the absence of C8. Elaboration of tissue factor messenger RNA was observed over a period of 8-30 h and required protein synthesis. Expression of tissue factor was not a direct consequence of the action of C on the EC but was a secondary response that required as an intermediate step the release of interleukin 1 alpha, an early product of the EC response to C activation. These findings suggest that, after the assembly of membrane attack complex on EC, the production of tissue factor and initiation of coagulation in a blood vessel depend on the production of interleukin 1 alpha and on its availability to stimulate affected EC.

scholarly journals Procoagulant Phospholipids and Tissue Factor Activity in Cerebrospinal Fluid from Patients with Intracerebral Haemorrhage

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Patrick Van Dreden ◽  
Guy Hue ◽  
Jean-François Dreyfus ◽  
Barry Woodhams ◽  
Marc Vasse
Keyword(s):  
Cerebrospinal Fluid ◽  
Tissue Factor ◽  
Intracerebral Haemorrhage ◽  
Factor Xa ◽  
Viral Meningitis ◽  
Brain Diseases ◽  
Coagulation Cascade ◽  
Factor Activity ◽  
Tissue Factor Activity ◽  
Home Test

Brain contains large amounts of tissue factor, the major initiator of the coagulation cascade. Neuronal apoptosis after intracerebral haemorrhage (ICH) leads to the shedding of procoagulant phospholipids (PPLs). The aim of this study was to investigate the generation of PPL, tissue factor activity (TFa), and D-Dimer (D-Di) in the cerebrospinal fluid (CSF) at the acute phase of ICH in comparison with other brain diseases and to examine the relationship between these factors and the outcome of ICH. CSF was collected from 112 patients within 48 hours of hospital admission. Thirty-one patients with no neurological or biochemical abnormalities were used to establish reference range in the CSF (“controls”). Thirty had suffered an ICH, and 51 other neurological diagnoses [12: ventricular drainage following brain surgery, 13: viral meningitis, 15: bacterial meningitis, and 11 a neurodegenerative disease (NDD)]. PPL was measured using a factor Xa-based coagulation assay and TFa by one home test. PPL, D-Di, and TFa were significantly higher (P<0.001) in the CSF of patients with ICH than in controls. TFa levels were significantly (P<0.05) higher in ICH than in patients with meningitides or NDD. Higher levels (P<0.05) of TFa were observed in patients with ICH who died than in survivors. TFa measurement in the CSF of patients with ICH could constitute a new prognostic marker.

Studies of the Mechanism for Enhanced Cell Surface Factor VIIa/Tissue Factor Activation of Factor X on Fibroblast Monolayers after Their Exposure to N-Ethylmaleimide

1994 ◽  
Vol 72 (06) ◽  
pp. 848-855 ◽  
Author(s):  
Dzung The Le ◽  
Samuel I Rapaport ◽  
L Vijaya Mohan Rao
Keyword(s):  
Cell Surface ◽  
Tissue Factor ◽  
Factor Viia ◽  
Cell Damage ◽  
Specific Binding ◽  
Surface Membrane ◽  
Annexin V ◽  
Factor X ◽  
Binding Studies ◽  
Anionic Phospholipid

SummaryFibroblast monolayers constitutively expressing surface membrane tissue factor (TF) were treated with 0.1 mM N-ethylmaleimide (NEM) for 1 min to inhibit aminophospholipid translocase activity without inducing general cell damage. This resulted in increased anionic phospholipid in the outer leaflet of the cell surface membrane as measured by the binding of 125I-annexin V and by the ability of the monolayers to support the generation of prothrombinase. Specific binding of 125I-rVIIa to TF on NEM-treated monolayers was increased 3- to 4-fold over control monolayers after only brief exposure to 125I-rVIIa, but this difference progressively diminished with longer exposure times. A brief exposure of NEM-treated monolayers to rVIIa led to a maximum 3- to 4-fold enhancement of VIIa/TF catalytic activity towards factor X over control monolayers, but, in contrast to the binding studies, this 3- to 4-fold difference persisted despite increasing time of exposure to rVIIa. Adding prothrombin fragment 1 failed to diminish the enhanced VIIa/TF activation of factor X of NEM-treated monolayers. Moreover, adding annexin V, which was shown to abolish the ability of NEM to enhance factor X binding to the fibroblast monolayers, also failed to diminish the enhanced VIIa/TF activation of factor X. These data provide new evidence for a possible mechanism by which availability of anionic phospholipid in the outer layer of the cell membrane limits formation of functional VIIa/TF complexes on cell surfaces.

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