Faculty Opinions recommendation of The immunoconjugate "icon" targets aberrantly expressed endothelial tissue factor causing regression of endometriosis.

2010 ◽  
Author(s):  
Sun-Wei Guo
Keyword(s):  
Tissue Factor ◽  
Endothelial Tissue

Induction of Endothelial Tissue Factor by Endotoxin and Its Precursors

1993 ◽  
Vol 70 (04) ◽  
pp. 702-706 ◽  
Author(s):  
Charles F Moldow ◽  
Ronald R Bach ◽  
Katherine Staskus ◽  
Paul D Rick
Keyword(s):  
Tissue Factor ◽  
Lipid A ◽  
Umbilical Vein ◽  
Structural Determinants ◽  
Monophosphoryl Lipid A ◽  
Maximal Induction ◽  
Umbilical Vein Endothelial Cells ◽  
Acyloxyacyl Hydrolase ◽  
Endothelial Tissue ◽  
Specific Mrna

SummaryThe structural determinants of lipopolysaccharide required for the induction of tissue factor in human umbilical vein endothelial cells were studied. Intact lipid A was essential for the induction of tissue factor whereas the incomplete lipid A precursors lipid IVA and lipid X, as well as monophosphoryl lipid A and acyloxyacyl hydrolase-treated lipopolysaccharide, were unable to induce tissue factor and tissue factor specific mRNA. However, the lipid A precursor, lipid IVA, was able to inhibit LPS-mediated induction of tissue factor; structural determinants distal to lipid A were found to be required for maximal induction of tissue factor activity and tissue factor mRNA. The presence of serum in the assay was found to amplify but was not obligate for tissue factor induction by LPS.

scholarly journals Caffeic Acid Phenethyl Ester Inhibits Endothelial Tissue Factor Expression

2013 ◽  
Vol 36 (6) ◽  
pp. 1032-1035 ◽  
Author(s):  
Cathérine Gebhard ◽  
Barbara Elisabeth Stähli ◽  
Stephanie Largiadèr ◽  
Erik Walter Holy ◽  
Alexander Akhmedov ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Caffeic Acid ◽  
Caffeic Acid Phenethyl Ester ◽  
Tissue Factor Expression ◽  
Factor Expression ◽  
Endothelial Tissue

scholarly journals Proteomic analysis of factors secreted by glioblastoma that induce endothelial tissue factor

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Daniel J Brat ◽  
Carol Tucker‐Burden ◽  
Yuan Rong ◽  
Gang Chen ◽  
Don Durden ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Proteomic Analysis ◽  
Endothelial Tissue

EFFECT OF PORCINE ENDOTHELIAL TISSUE FACTOR PATHWAY INHIBITOR ON HUMAN COAGULATION FACTORS1

1997 ◽  
Vol 63 (5) ◽  
pp. 749-758 ◽  
Author(s):  
Christoph W. Kopp ◽  
Jonathan B. Siegel ◽  
Wayne W. Hancock ◽  
Josef Anrather ◽  
Hans Winkler ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Tissue Factor Pathway ◽  
Endothelial Tissue

The Blood Monocyte - TNF - Endothelial Axis in Activation of Endothelial Tissue Factor in the Transgenic Sickle Mouse: Possible Relevance of Etanercept to Sickle Coagulopathy

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1048-1048
Author(s):  
Anna Solovey ◽  
Liming Milbauer Chang ◽  
Fuad Abdulla ◽  
Rahn Kollander ◽  
Paul H Marker ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Conflicts Of Interest ◽  
Pulmonary Veins ◽  
Ambient Air ◽  
Blood Monocytes ◽  
Extended Treatment ◽  
Pre Treatment ◽  
Endothelial Tissue

Abstract Abstract 1048 Peripheral blood monocytes can be pathogenic participants in vascular disease, and they are abnormally activated in sickle patients. As shown earlier, sickle mice have abnormally increased expression of endothelial tissue factor (eTF) in pulmonary veins (PV), expressed as % of PV positive for eTF. For HbS-BERK (eTF 36%, vs 9% for HbA-BERK controls) and S+SAntilles (eTF 28%, vs 7% for C57BL6 controls), abnormal eTF expression is chronic. For NY1DD, however, eTF switches from 7% at ambient air to 23% after exposure to hypoxia/reoxygenation (post-H/R). Having now examined roles of transcription factors Egr-1 and NFkB(p50), we find that H/R triggered expression of eTF in post-H/R NY1DD is: [a] dependent upon both Egr-1 and NFkB(p50) within peripheral blood mononuclear cells (PBMC), and dependent upon Egr-1 butnot NFkB(p50) in vessel wall endothelium. To examine the roles of PBMC and their product TNF in activating eTF expression we used three strategies. [A] First, transfusion (Tx) of PBMC from donor mice (DM) induced eTF in recipient mice (RM) as follows. At-air NY1DD RM exhibited eTF of 7% from Tx of at-air NY1DD DM PBMC, and eTF of 19% from Tx of post-H/R NY1DD DM PBMC. C57BL6 RM exhibited eTF of 10% from Tx of C57BL6 DM PBMC, 31% from Tx of S+SAntilles DM PBMC, and only 15% from Tx of PBMC from S+SAntilles DM also having NFkB(p50)−/−. HbA-BERK RM exhibited eTF of 9% from Tx of HbA-BERK DM PBMC, and 36% from Tx of HbS-BERK DM PBMC. [B] Second, we examined effect of TNF+LT blocker etanercept on PBMC in transfusion experiments. As expected, HbA-BERK RM exhibited eTF 36% from Tx of HbS-BERK PBMC obtained from etanercept-treated (3 mg/kg × 2) DM, and 38% from Tx of HbS-BERK PBMC obtained from DM treated with inactive control TNF-R-scrambled-peptide. On the other hand, HbA-BERK RM pre-treated with etanercept (same dose) vs control TNF-R-scrambled-peptide exhibited eTF of 11% and 33%, respectively from Tx of HbS-BERK DM PBMC. [C] Third, direct TNF blocking pre-treatment of NY1DD mice prevented the eTF increase from subsequent H/R (to 23% for the no pre-treatment controls): eTF of 5% (P=.000013) for pre-treatment with high-etanercept (10 mg/kg × 2), 12% (P=.00059) for pre-treatment with low-etanercept (3 mg/kg × 2), 19% (P=.053) for pre-treatment with IL1-blocker anakinra (10 mg/kg ×2), and 7% (P=.0016) for pretreatment withTNF-specific blocker infliximab (10 mg/kg ×2). For HbS-BERK mice having pre-existing eTF of 36%, extended treatment with etanercept (3 mg/kg, twice weekly × 3) reduced eTF to 27% (P=.026) while those receiving scrambled-peptide remained at 34%. Higher or longer etanercept may be more effective. Other murine treatments have shown us reversal of pre-existing eTF requires extended treatment. Since regulation of TF expression in endothelial cells and blood monocytes is similar, it is likely that these eTF effects would be paralleled by similar effects on monocyte TF expression. Thus, these results suggest that TNF blocking strategies could be helpful in mitigating effects of coagulation activation in the sickle context. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Paclitaxel Enhances Thrombin-Induced Endothelial Tissue Factor Expression via c-Jun Terminal NH 2 Kinase Activation

2006 ◽  
Vol 99 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Barbara E. Stähli ◽  
Giovanni G. Camici ◽  
Jan Steffel ◽  
Alexander Akhmedov ◽  
Kushiar Shojaati ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Expression ◽  
Kinase Activation ◽  
Factor Expression ◽  
Endothelial Tissue
Sign in / Sign up

Export Citation Format

Share Document