Tissue Factor Activity of Syncytiotrophoblast Plasma Membranes and Tumoral Trophoblast Cells in Culture

Reverdiau, Pascale; Jarousseau, A C; Thibault, Gilles; Khalfoun, B.; Watier, Hervé; Lebranchu, Yvon; Bardos, P.; Gruel, Yves

doi:10.1055/s-0038-1653724

Cited by 33 publications

(31 citation statements)

References 30 publications

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“…Corroborating earlier reports, 42 both cell lines expressed high levels of TF activity (data not shown) and initiated intracellular calcium signals upon PAR1 and PAR2 activation (data not shown). Akin to murine trophoblast cells, PAR1 activation resulted in a 13-fold increase in EGR1 mRNA and a 5-fold increase in CYR61 mRNA expression in human Jeg3 cells ( Figure S2).…”

Section: Cross-species Conservation Of Trophoblast Gene Expression Insupporting

confidence: 91%

Fetomaternal cross talk in the placental vascular bed: control of coagulation by trophoblast cells

Sood

Kalloway

Mast

et al. 2006

Blood

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IntroductionIn the hemochorial type of placentation observed in humans and mice, fetal nutrition involves the direct uptake of nutrients by zygote-derived trophoblast cells from circulating maternal blood. The required placental morphology is achieved through a highly regulated process of trophoblast differentiation coupled with remodeling of maternal and fetal vasculature. As a consequence, in contrast to all other vascular beds in which the blood vessel endothelium is the principal gatekeeper between tissue and blood, the terminal vascular space of the placenta is lined by trophoblast cells. 1,2 Trophoblast cells are genetically distinct from the maternal vascular endothelium and are derived from a different developmental lineage than endothelial cells. 3 In all nonplacental vascular beds, normal endothelium proactively suppresses the activity of the coagulation system, thereby maintaining a nonthrombogenic surface. A survey of existing data suggests that trophoblast cells also produce endothelial regulators of hemostasis, such as thrombomodulin (TM), endothelial protein C receptor (EPCR), and tissue factor pathway inhibitor (TFPI). [4][5][6][7][8] Such findings indicate that trophoblast cells might exhibit an endothelial cell-like ability to partake in the regulation of hemostasis at the fetomaternal interface. Indeed, the term "endothelial mimicry" has been coined to describe a process of remodeling of the maternal arteries, during which so-called "endovascular" trophoblast cells replace the maternal endothelium in these blood vessels and switch their expression from epithelial to endothelial adhesion receptor repertoire. [9][10][11] It is unknown whether trophoblast cells acquire anticoagulant gene expression in a temporally and spatially controlled manner similar to that described for the subset of endovascular trophoblast cells or whether the acquisition of an endothelial cell-like anticoagulant phenotype is a cell type-defining feature of trophoblast cells in general.The placenta also is a rich source of the initiator of coagulation, tissue factor (TF). TF antigen and procoagulant activity are detected in mouse giant and labrynthine trophoblasts and on human syncytiotrophoblast membranes. [12][13][14][15] With the exception of angiogenic endothelium, and in endothelium subjected to inflammatory and thrombotic stimuli, TF expression is strictly excluded from endothelial cells. Proinflammatory cytokines, ligands for Tollreceptors, and the principal coagulation protease, thrombin, induce TF expression in cultured endothelial cells, evoke increased production of endothelial-leukocyte adhesion receptors, and simultaneously suppress the expression of anticoagulant gene products. This transition from a noncoagulant and antiadhesive phenotype to a state of enhanced coagulation and leukocyte interactions has been termed "endothelial activation" and appears to reflect a principal switch in a concerted gene-expression program. 16 In contrast, trophoblast cells constitutively express TF, thus exhibiting, even under ...

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Section: Cross-species Conservation Of Trophoblast Gene Expression Insupporting

confidence: 91%

Fetomaternal cross talk in the placental vascular bed: control of coagulation by trophoblast cells

Sood

Kalloway

Mast

et al. 2006

Blood

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“…This basal activity of cultured endothelial cells probably reflects phenotypic changes upon removal of these cells from their native environment under flow. 44 Regardless, the observed differences between fibrin networks formed by endothelial cells and extravascular cells are profound, and suggest exposure of extravascular cells to blood would promote a stable fibrin network after vascular injury.…”

Section: Discussionmentioning

confidence: 99%

Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability

Campbell

Overmyer

Selzman

et al. 2009

Blood

132

159

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Fibrin is essential for hemostasis; however, abnormal fibrin formation is hypothesized to increase thrombotic risk. We previously showed that in situ thrombin generation on a cell's surface modulates the 3-dimensional structure and stability of the fibrin network. Currently, we compared the abilities of extravascular and intravascular cells to support fibrin formation, structure, and stability. Extravascular cells (fibroblasts, smooth muscle) supported formation of dense fibrin networks that resisted fibrinolysis, whereas unstimulated intravascular (endothelial) cells produced coarse networks that were susceptible to fibrinolysis. All 3 cell types produced a fibrin structural gradient, with a denser network near, versus distal to, the cell surface. Although fibrin structure depended on cellular procoagulant activity, it did not reflect interactions between integrins and fibrin. These findings contrasted with those on platelets, which influenced fibrin structure via interactions between ␤3 integrins and fibrin. Inflammatory cytokines that induced prothrombotic activity on endothelial cells caused the production of abnormally dense fibrin networks that resisted fibrinolysis. Blocking tissue factor activity significantly reduced the density and stability of fibrin networks produced by cytokine-stimulated endothelial cells. Together, these findings indicate fibrin structure and stability reflect the procoagulant phenotype of the endogenous cells, and suggest abnormal fibrin structure is a novel link between inflammation and thrombosis. (Blood. 2009;114:4886-4896)

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“…Moreover, increased apoptosis of extravillous trophoblast in pre-eclampsia has also been observed 26,27 . Abnormally high rates of apoptosis may account for defective invasion of trophoblast, leading to failure of physiological transformation of the spiral arteries 27,60 or thrombosis by the activation of the hemostatic system by trophoblast fragments [36][37][38] .…”

Section: Discussionmentioning

confidence: 99%

“…A high rate of apoptosis in villous trophoblast may lead to deportation of trophoblast cells into the maternal circulation, while the increased cell death may explain defective trophoblast invasion of the decidua and spiral arteries (abnormal placentation), as well as activation of the hemostatic system in patients with preeclampsia 26,[36][37][38] . The factor(s) responsible for enhanced trophoblast apoptosis in pre-eclampsia have not been determined.…”

Section: Introductionmentioning

confidence: 99%

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Neale

Demasio

Illuzi

et al. 2003

The Journal of Maternal-Fetal & Neonatal Medicine

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Tissue Factor Activity of Syncytiotrophoblast Plasma Membranes and Tumoral Trophoblast Cells in Culture

Cited by 33 publications

References 30 publications

Fetomaternal cross talk in the placental vascular bed: control of coagulation by trophoblast cells

Fetomaternal cross talk in the placental vascular bed: control of coagulation by trophoblast cells

Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

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