Inhibitors of Phosphodiesterase (Pentoxifylline, Trequinsin) Inhibit Apical and Subcellular Matrix Expression of Tissue Factor in Cultured Human Endothelial Cells

Leclerc, Nathalie; Haan-Archipoff, Gisèle; Lenoble, Michèle; Beretz, Alain

doi:10.1097/00005344-199500252-00019

Cited by 7 publications

(1 citation statement)

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“…16,23,24,28,36,49,55 The negative correlation of TF expression with intracellular cAMP level has been reported in many cells [56][57][58][59][60][61] (Table 1) 65 Angiopoietin downregulates TF expression. 74 The antisense interference with RNA or DNA downregulates TF transcription in vitro 75 and in vivo.…”

Section: Tf Upregulation Responsible For Hypercoagulabilitymentioning

confidence: 99%

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Chu

2006

Cell Biochem. Funct.

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The extrinsic coagulation is recognized as an 'inducible' signalling cascade resulting from tissue factor (TF) upregulation by exposure to clotting zymogen FVII upon inflammation or tissue injury. Following the substantial initiation, an array of proteolytic activation generates mediating signals (active serine proteases: FVIIa, FXa and FIIa) that lead to hypercoagulation with fibrin overproduction manifesting thrombosis. In addition, TF upregulation plays a central role in driving a thrombosis-inflammation circuit. Coagulant mediators (FVIIa, FXa and FIIa) and endproduct (fibrin) are proinflammatory, eliciting tissue necrosis factor, interleukins, adhesion molecules and many other intracellular signals in different cell types. Such resulting inflammation could ensure 'fibrin' thrombosis via feedback upregulation of TF. Alternatively, the resulting inflammation triggers platelet/leukocyte/polymononuclear cell activation thus contributing to 'cellular' thrombosis. TF is very vulnerable to upregulation resulting in hypercoagulability and subsequent thrombosis and inflammation, either of which presents cardiovascular risks. The prevention and intervention of TF hypercoagulability are of importance in cardioprotection. Blockade of inflammation reception and its intracellular signalling prevents TF expression from upregulation. Natural (activated protein C, tissue factor pathway inhibitor, or antithrombin III) or pharmacological anticoagulants readily offset the extrinsic hypercoagulation mainly through FVIIa, FXa or FIIa inhibition. Therefore, anticoagulants turn off the thrombosis-inflammation circuit, offering not only antithrombotic but anti-inflammatory significance in the prevention of cardiovascular complications.

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Section: Tf Upregulation Responsible For Hypercoagulabilitymentioning

confidence: 99%

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Chu

2006

Cell Biochem. Funct.

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Tumor necrosis factor-α attenuates N-methyl-d-aspartate-mediated neurotoxicity in neonatal rat hippocampus

Liu

Barks

1999

Brain Research

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Chemistry of Pyrido[1,2-c] [1,3]oxazines, Pyrido[1,2-c][1,3]thiazines, Pyrido[1,2-c]pyrimidines, and Their Benzologs: Part II

Hermecz

1997

Advances in Heterocyclic Chemistry

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Inhibitors of Phosphodiesterase (Pentoxifylline, Trequinsin) Inhibit Apical and Subcellular Matrix Expression of Tissue Factor in Cultured Human Endothelial Cells

Cited by 7 publications

References 0 publications

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Tissue factor upregulation drives a thrombosis–inflammation circuit in relation to cardiovascular complications

Tumor necrosis factor-α attenuates N-methyl-d-aspartate-mediated neurotoxicity in neonatal rat hippocampus

Chemistry of Pyrido[1,2-c] [1,3]oxazines, Pyrido[1,2-c][1,3]thiazines, Pyrido[1,2-c]pyrimidines, and Their Benzologs: Part II

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