Cryptic messages: Is noncoagulant tissue factor reserved for cell signaling?

Camerer, Eric; Trejo, JoAnn

doi:10.1073/pnas.0606888103

Cited by 11 publications

(6 citation statements)

References 17 publications

(12 reference statements)

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“…De-encryption, i.e. without a change in TF mRNA or protein, occurs in response to a number of stimuli, including cell damage, proteases, phospholipases, apoptosis, complement and calcium ionophores [29,31]. Despite the evidence for a rapid increase in coagulation and fibrin formation following damage, we were unable to detect a change in TF activity, measured as the generation of active Xa, with wounding.…”

Section: Discussioncontrasting

confidence: 69%

“…TF exists in microdomains on the cell surface with a mixed population of active and encrypted protein, encrypted meaning that while the TF antigen is detectable on the surface of unactivated cells, its full pro-coagulant activity is not [29]. FVIIa is able to bind to both encrypted and de-encrypted TF, but when the TF is encrypted the TF/FVIIa complex activates cell signalling, but does not activate FVII/FX and subsequent coagulation [30,31]. De-encryption, i.e.…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Fibrin formation by wounded bronchial epithelial cell layers in vitro is essential for normal epithelial repair and independent of plasma proteins

Perrio

Ewen

Trevethick

et al. 2007

Clin Experimental Allergy

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Section: Discussioncontrasting

confidence: 69%

Section: Discussionmentioning

confidence: 98%

Fibrin formation by wounded bronchial epithelial cell layers in vitro is essential for normal epithelial repair and independent of plasma proteins

Perrio

Ewen

Trevethick

et al. 2007

Clin Experimental Allergy

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“…29) Active TF binds factors VIIa and Xa, and cleaves and activates PAR-2, and soluble Xa mediates PAR1. 30,31) By blocking PAR-1 and PAR-2 with rivaroxaban, the production of several inflammatory cytokines, such as TIMP-1, I-309, IL-16, IL-2, I-TAC, M-CSF, MCP-5, SDF-1, and TNF-α, were significantly inhibited in Ang II-induced CFs. These inflammatory mediators are expected to accelerate cell migration and proliferation in activated CFs.…”

Section: Discussionmentioning

confidence: 99%

Rivaroxaban Inhibits Angiotensin II-Induced Activation in Cultured Mouse Cardiac Fibroblasts Through the Modulation of NF-<i>κ</i>B Pathway

et al. 2015

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Cell migration, proliferation, and differentiation of cardiac fibroblasts (CFs) play a central role in cardiac fibrosis. Factor Xa (FXa)-dependent protease-activated receptor (PAR)-1 and PAR-2 have been reported as important targets in proinflammatory and fibroproliferative diseases. From this viewpoint, we aimed to investigate whether treatment of rivaroxaban, an approved oral direct FXa inhibitor, attenuates functional changes in angiotensin (Ang) II-induced mouse CFs.Confluent cultured mouse CFs were pretreated with or without rivaroxaban. Ang II-induced cell migration was decreased by 73% in rivaroxaban induced cells. Rivaroxaban inhibited Ang II-induced cell proliferation by 27% at 0.01 μg/ mL, 69% at 0.1 μg/mL, 71% at 1 μg/mL, and 69% at 5 μg/mL. In mouse cytokine array measuring 40 cytokines, the productions of interleukin-16, TIMP-1, and tumor necrosis factor-α (TNF-α) were significantly reduced with 0.1 μg/mL of rivaroxaban pretreatment (all P < 0.05). TIMP-1 levels in the culture supernatant measured by ELISA were also decreased by rivaroxaban pretreatment in Ang II-induced CFs (35% decrease at 0.01 μg/mL, 47% at 0.1 μg/mL, 47% at 1 μg/mL, and 57% at 5 μg/mL). In the dual reporter assay analysis, rivaroxaban inhibited various inflammatory signal pathways, including the nuclear factor-kappa B (NF-κB), active protein-1 (AP-1), and mitogen-activated protein kinase (MAPK) pathways (decreases of 82%, 78%, and 75%, respectively).These data suggest that rivaroxaban inhibits Ang II-induced functional activation in cultured mouse CFs via inhibiting NF-κB and MAPK/AP-1 signaling pathways, which may be a possible target of heart failure, through the antifibrotic and anti-inflammatory efficacy of rivaroxaban in Ang II-stimulated cardiac fibroblasts.

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“…Tissue factor is required for normal uterine hemostasis, and PAR‐2 increases the number of leukocytes and MMP‐7 expression during the menstrual cycle . Increased TF and PAR‐2 action in ectopic endometrium may augment expression of VEGF and proinflammatory substances which further promote the development of endometriosis . In contrast to decreased expression of the TF and PAR‐2 in endometrium without endometriosis, eutopic endometrium with endometriosis expresses similar levels of TF and PAR‐2 to those in ectopic lesions.…”

Section: Discussionmentioning

confidence: 99%