The Role of Endothelial Cells and Subendothelial Components in the Initiation of Blood Coagulation

Østerud, Bjarne

doi:10.1159/000214322

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…The phospholipid-dependent way is not limited; possibly the cells have factor Xa bypassing activity. Osterud described an enhanced formation of factor Xa and thrombin by lyzed EC which was not caused by the activity of tissue factor (8). Thrombin generation both in the presence of Ca+ + and of cephalin is more effective when using EC than when using SMC in the test system.…”

Section: Discussionmentioning

confidence: 98%

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

Kirchhof

Grünwald

1982

Thromb Haemost

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SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.

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Section: Discussionmentioning

confidence: 98%

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

Kirchhof

Grünwald

1982

Thromb Haemost

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“…Following cellular activation or injury, EC express TF-Ag which is predominantly associated with the subendothelial matrix and which becomes exposed to coagulation factors after EC injury and retraction in vivo (8)(9)(10)(11). EC are a major source of constitutive TFPI, that is upregulated by TNF␣, IL-1 and phorbol ester in vitro (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Monocyte Tissue Factor Activity by Allogeneic and Xenogeneic Endothelial Cells

Kopp¹,

Siegel²,

Anrather³

et al. 1998

Thromb Haemost

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SummaryThe regulation of tissue factor (TF) activity by the cell associated tissue factor pathway inhibitor (TFPI) during monocyte (Mo) and endothelial cell (EC) interactions is not fully understood. This report describes co-ordinate induction of TF antigen (TF-Ag) and membrane-associated TFPI-Ag on human Mo following coculture with human aortic (HAEC) or porcine aortic EC (PAEC) or after stimulation with TNFα. We show that both allo- and xenogeneic EC induce human Mo-TF antigen in short-term culture. However, the TF activity of TNFα-primed Mo is suppressed when these cells are cocultured with HAEC [by 40.3 ± 6.3% (p <0.02)] or PAEC [by 50.5 ± 10.6% (p <0.001)]. Antibody (Ab) blocking studies confirm that TFPI is the principal anticoagulant associated with this suppression of TF-activity. Our data indicate that anti-TF activity originates, at least in part, from the activated human Mo in the coculture; additionally, specific generation of TFPI by Mo is observed under the xenogeneic culture conditions. As Mo associated TF, induced by allo- or xenogeneic EC interactions, is regulated by cell-associated TFPI, we propose that infiltrating Mo may modulate the thrombotic process at sites of vascular injury in association with both allo- and xenograft rejection.Aspects of the work were presented at the American Society for Hematology meeting in Orlando, FL, December 1996.

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“…More likely, the release of several activators from leukocytes [20,22,24,25,30,35], plate lets [29. 30] and endothelial cells [11,26,34] leads to specific activation of the above-mentioned blood systems resulting in severe consumption (DIC) of the involved proteins. Besides this drastic activation followed by elimi nation of the plasma proteins via complex formation with inhibitors (in the case of the blood system proteinases) or specific degradation (e.g.…”

Section: Introductionmentioning

confidence: 99%

Clotting and Other Plasma Factors in Experimental Endotoxemia: Inhibition of Degradation by Exogenous Proteinase Inhibitors

Jochum¹,

Witte²,

Schießler³

et al. 1981

Eur Surg Res

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Endotoxemia in dogs was induced by a slow intravenous infusion of E. coli endotoxin for 2 h. Thereby, a significant decrease was observed in the plasma levels of several clotting, fibrinolysis and complement factors. The changes were studied over an experimental period of 14 h and checked for statistical significance by three-way analysis of variance. Application of the broad-spectrum proteinase inhibitor aprotinin (Trasylol®) from bovine organs clearly lowered the endotoxin-induced decline of the plasma proteins studied. By intravenous application of a specific granulocytic proteinase inhibitor (Bow-man-Birk inhibitor from soybeans), the endotoxin-induced reduction of the plasma proteins was prevented in a similar manner. It can be concluded that at least some of the pathobiochemical mechanisms observed in clotting, fibrinolysis and complement systems during endotoxemia are not only caused by a severe consumption reaction but also by unspecific proteolytic degradation due to neutral granulocytic proteinases.

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The Role of Endothelial Cells and Subendothelial Components in the Initiation of Blood Coagulation

Cited by 3 publications

References 6 publications

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

Regulation of Monocyte Tissue Factor Activity by Allogeneic and Xenogeneic Endothelial Cells

Clotting and Other Plasma Factors in Experimental Endotoxemia: Inhibition of Degradation by Exogenous Proteinase Inhibitors

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