Effects of Binding of Ligand (FVIIa) to Induced Tissue Factor in Human Endothelial Cells

Wiiger, Merete Thune; Pringle, S; Pettersen, Kjell Sverre; Narahara, Nobuhiro; Prydz, Hans

doi:10.1016/s0049-3848(00)00183-3

Cited by 8 publications

(7 citation statements)

References 34 publications

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“…TFPI is released from EC and indicates EC injury 23 . FVIIa is responsible for initiating blood coagulation in normal hemostasis and thrombotic disorders 24 . F1 + 2 is released from prothrombin during its conversion to thrombin by prothrombinase complex and reflects activation of blood coagulation 25 .…”

Section: Discussionmentioning

confidence: 99%

Absence of hypercoagulability in acute Kawasaki disease

Lin∥

Tsao²,

Cheng

et al. 2005

Pediatrics International

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Section: Discussionmentioning

confidence: 99%

Absence of hypercoagulability in acute Kawasaki disease

Lin∥

Tsao²,

Cheng

et al. 2005

Pediatrics International

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“…We used cell lines with constitutive TF expression (porcine aorta endothelial cell line transfected with human TF and PDGFR␤, and human foreskin fibroblasts 1064Sk), and freshly isolated lipopolysaccharide (LPS)-stimulated human monocytes. 3,12,24 We show that TF/FVIIa engages in a cross-talk with PDGFR␤ by selectively potentiating the response of the cells to PDGF-BB differently from 5 other chemotactic agents. This potentiation is regulated by PAR-2, c-Src and c-Yes kinases, and PLC isoform(s) other than PLC␥1 and PLC␤3, but not by MAP kinases.…”

mentioning

confidence: 86%

TF/FVIIa Transactivate PDGFRβ to Regulate PDGF-BB–Induced Chemotaxis in Different Cell Types

Siegbahn

Johnell

Nordin

et al. 2008

ATVB

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Background-We have previously reported the potentiation of PDGF-BB-induced chemotaxis of fibroblasts, vascular smooth muscle cells, and endothelial cells by FVIIa. Here we studied the role of TF/FVIIa and the induced signaling pathways in regulation of chemotaxis of human monocytes, fibroblasts, and porcine aorta endothelial cells. Methods and Results-Human monocytes were obtained by using Ficoll-Paque gradient and the MACS system (for highly purified population), fibroblasts and PAE cells have been characterized previously. Inhibitors of selected signaling intermediates were used, and the effect of TF/FVIIa on the migratory response of all cells to chemotactic agents was analyzed.The induced signaling was studied by immunoprecipitation and Western blotting. TF/FVIIa complex selectively enhanced PDGF-BB-induced chemotaxis in a Src-family, PLC, and PAR-2-dependent manner. Using PAE cells we identified c-Src and c-Yes as the Src-family members activated by TF/FVIIa. We report for the first time the PAR-2 and Src family-dependent transactivation of PDGFR␤ by TF/FVIIa involving phosphorylation of a subset of PDGFR␤ tyrosines. Conclusions-The

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“…Furthermore, the complexity is increased by the observation that the stability of TF can be modulated. In interleukin (IL)-1 stimulated endothelial cells, the half life of TF is reduced in the presence of FVII(a) (70), an example of a cell biological function of the TF-FVII(a) interaction.…”

Section: Introductionmentioning

confidence: 99%

Tissue Factor – A Receptor Involved in the Control of Cellular Properties, Including Angiogenesis

Jiang¹,

Bierhaus²,

Schiekofer³

et al. 2001

Thromb Haemost

110

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SummaryTissue factor (TF), the major initiator of blood coagulation, serves as a regulator of angiogenesis, tumor growth and metastasis. In several models, TF expression mediates upregulation of the proangiogenic vasular endothelial growth factor (VEGF) that can directly act on endothelial cells to promote vessel formation. This occurs through ligand binding, activation of signaling cascades, signal transduction and alteration of growth factor expression and is mediated by both, coagulation-dependent and -independent pathways. Depending on the cell type and the biological settings, TF seems to affect cellular properties through (i) factor VIIa (FVIIa)-dependent proteolysis of factor Xa (FXa) and thrombin and subsequent activation of proteinase activated receptor (PAR) -1 and PAR-2, (ii) through direct FVIIa signaling and mitogen activated protein (MAP) kinase activation, that is conferred by a not yet identified receptor, (iii) through interaction of FVII(a) proteolytic activity and signaling of the cytoplasmic domain and (iv) through cytoplasmic signaling independent of ligand binding. The role of phosphorylation of the cytoplasmic domain and the pathways controlling phosphorylation of TF remain poorly understood.

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Effects of Binding of Ligand (FVIIa) to Induced Tissue Factor in Human Endothelial Cells

Cited by 8 publications

References 34 publications

Absence of hypercoagulability in acute Kawasaki disease

Absence of hypercoagulability in acute Kawasaki disease

TF/FVIIa Transactivate PDGFRβ to Regulate PDGF-BB–Induced Chemotaxis in Different Cell Types

Tissue Factor – A Receptor Involved in the Control of Cellular Properties, Including Angiogenesis

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