-
Higher TF activities are present in thinner abdominal aortic aneurysm regions. These parameters and local fibrinolysis may be part of the processes leading to destruction of the aneurysm wall.
-
The majority of plasma samples from burn patients have active FXIa and FIXa, with a significant fraction of them having active TF. The concentration of all three proteins varies in a wide range.
-
Alternatively spliced tissue factor levels are elevated in the plasma of patients with chronic liver diseases.
-
Increased plasma concentrations of TF in atrial fibrillation (AF) patients are accompanied and probably at least partly explained by increased levels of TF-bearing extracellular vesicles, which may be mechanistically involved in increased thrombogenicity in AF patients.
-
In diabetics, miR-19a and miR-126 cooperate to exhibit anti-thrombotic properties by epigenetic regulation of tissue factor.
-
High levels of TF were associated with thrombosis related to antiphospholipid syndrome.
-
Elevated plasma levels of procoagulant factors, such as FVIII or prothrombin, enhanced thrombin generation and reduced the amount of TF required for the initiation of thrombin formation.
-
TF knockout in MDA-MB-231cells reduced TF/FVIIa signaling and coagulation activity. Silencing of TF in MDA-MB-231cells decreased the release of microvesicles.
-
Subjects with AG and GG genotype had significantly higher TF levels than AA genotype. GG genotype of 603A>G polymorphism augments the risk of thrombosis by 4.4 fold, thus highlighting the significance of this polymorphism in the development of DVT
-
Monocyte TF may be a relevant source of TF-mediated thrombogenicity in NSCLC patients and may be associated with prognosis in NSCLC.
-
plasma activity higher in women with pre-eclampsia than in those with infants small for gestational age or normal pregnancies
-
The interaction between tissue factor and filamin A is dependent on the differential phosphorylation of Ser253 and Ser258. The interaction with filamin A may translocate cell surface TF to cholesterol-rich lipid rafts, increasing cell surface TF activity as well as TF incorporation and release into microvesicles.
-
The induction of TG by BXPC3 cells was mainly driven by the TF pathway while TG generation triggered by MCF7 cells was also driven by FXII activation.
-
Our study identifies a previously undescribed role of miRNA in venous thrombosis by regulating TF expression. Therefore, restoration of miR-145 levels may serve as a promising therapeutic strategy for management of venous thrombosis
-
TF(+) microvesicless released from orthotopic pancreatic tumors increase venous thrombosis in mice.
-
HUVEC and adult human dermal blood endothelial cells respond similarly to TNFalpha and IL-1beta in terms of TF expression, and both are suitable models to examine cell surface TF activity and TF-positive microvesicle release in endothelial cells.
-
Cell lines with intrinsically high TF expression were associated with decreased cancer stem cell activity. Knockdown of TF was associated with increased cancer stem cell activity. Overexpression of TF was associated with decreased cancer stem cell activity. Expression of TF did not affect cellular viability but may increase proliferation.
-
uPAR and TF could potentially be attractive targets for molecular imaging and therapy in oral squamous cell carcinoma due to high positive expression rates and tumor-specific expression patterns.
-
The highest tissue factor activity was detected in microparticles from monocytes, lower activity - in microparticles from endothelial cells and THP-1 cells, and no activity - in microparticles from platelets and granulocytes.
-
These results demonstrate that procoagulant microvesicles shed by head and neck squamous cell carcinoma line (UMSCC81B) induced a procoagulant effect in HUVECs through increased clotting activity and cell membrane surface expression of TF.
