Role of JAK2-STAT3 in TLR2-mediated tissue factor expression

2013 ◽  
Vol 114 (6) ◽  
pp. 1315-1321 ◽  
Author(s):  
Dae-Weon Park ◽  
Ji Hyo Lyu ◽  
Jin-Sik Kim ◽  
Haemin Chin ◽  
Yoe-Sik Bae ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Expression ◽  
Factor Expression

Functional role of Egr-1 mediating VEGF-induced tissue factor expression in the retinal capillary endothelium

2002 ◽  
Vol 240 (12) ◽  
pp. 1003-1010 ◽  
Author(s):  
Yukio Sassa ◽  
Yasuaki Hata ◽  
Toshinori Murata ◽  
Ichiro Yamanaka ◽  
Masae Honda ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Functional Role ◽  
Capillary Endothelium ◽  
Tissue Factor Expression ◽  
Retinal Capillary ◽  
Factor Expression

Role of tissue factor expression in thrombin generation by canine tumor cells

2016 ◽  
Vol 77 (4) ◽  
pp. 404-412 ◽  
Author(s):  
Erika J. Gruber ◽  
James L. Catalfamo ◽  
Tracy Stokol
Keyword(s):  
Tissue Factor ◽  
Tumor Cells ◽  
Thrombin Generation ◽  
Tissue Factor Expression ◽  
Factor Expression ◽  
Canine Tumor

Role of tissue factor expression on tumour cell invasion and growth of experimental pancreatic adenocarcinoma

1999 ◽  
Vol 86 (7) ◽  
pp. 890-894 ◽  
Author(s):  
A. K. Kakkar ◽  
V. Chinswangwatanakul ◽  
N. R. Lemoine ◽  
S. Tebbutt ◽  
R. C. N. Williamson
Keyword(s):  
Tissue Factor ◽  
Pancreatic Adenocarcinoma ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Tissue Factor Expression ◽  
Factor Expression ◽  
Tumour Cell Invasion

scholarly journals Role of the renin angiotensin system in TNF-α and Shiga-toxin-induced tissue factor expression

2007 ◽  
Vol 23 (2) ◽  
pp. 221-231 ◽  
Author(s):  
Eirini Nestoridi ◽  
Rafail I. Kushak ◽  
Olga Tsukurov ◽  
Eric F. Grabowski ◽  
Julie R. Ingelfinger
Keyword(s):  
Tissue Factor ◽  
Shiga Toxin ◽  
Renin Angiotensin System ◽  
Tissue Factor Expression ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Tnf Α ◽  
Factor Expression

Pivotal Role Of Heat Shock Proteins In Monocyte and Endothelial Cell Pathology In Sickle Cell Disease

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 969-969
Author(s):  
Nagavedi S. Umapathy ◽  
Kavita Natrajan ◽  
Abdullah Kutlar ◽  
Steffen E. Meiler ◽  
Julia E. Brittain
Keyword(s):  
Endothelial Cell ◽  
Tissue Factor ◽  
Cell Permeability ◽  
Ros Generation ◽  
Tissue Factor Expression ◽  
Monocyte Activation ◽  
Hsp90 Inhibitors ◽  
Hsp90 Inhibition ◽  
Factor Expression

Abstract Background It is well established that sickle cell disease (SCD) manifests global perturbations of hemostasis. Vaso-occlusion, inflammation and coagulopathy all likely contribute to the protean complications of SCD. Central to both inflammation and coagulation is the monocyte. These cells can be profoundly pro-inflammatory and can express tissue factor on their surface and thus influence both inflammation and coagulation. Monocytosis is common in SCD, as is steady state monocyte activation. Exaggerated monocytic response to stimulus may also contribute to the severity of acute events. Thus, agents that regulate monocyte function are potentially of significant relevance in SCD. To this end, we have discovered that the heat shock proteins (HSPs) are potential master regulators of these cells. We previously demonstrated that inhibition of one such HSP, HSP90, could completely ablate the profound and hyper-responsive monocytic inflammatory release upon lipopolysacchiride (LPS) challenge. Inhibition of HSP90 also blocked LPS induced NFk-B translocation to the nucleus. Thus, these results suggested a potent role for HSP90 in LPS-induced monocyte based inflammation. However, the role of HSP90 is cytokine-induced monocyte activation was speculative. The role of HSP90 in monocyte tissue factor expression, or reactive oxygen species (ROS) generation remained unknown. Objectives We sought to determine the role of HSP90 in regulating the pro-inflammatory, pro-coagulant, and ROS generating potential in monocytes. We then wanted to establish a potential role for HSP90 inhibition. Methods Peripheral blood mononuclear cells (PBMCs) were isolated from whole blood using Ficoll density separation. Flow cytometry was employed to measure the LPS- or cytokine-induced monocyte tissue factor expression and ROS generation. Monocyte ROS generation was detected using L012 based chemiluminescence or visualized in individual cells using flow cytometry with CELLROX. Inflammatory cytokines and tissue factor gene expression was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). NFkB translocation to the nucleus was detected via cell fractionation followed by western blotting or indirect immunofluorescence. PBMCs or THP-1 cells were pre-treated with the HSP90 inhibitors 17-DMAG or AUY922 prior to assay. Monocyte- induced endothelial cell permeability was measured using endothelial cell-substrate impedance sensing (ECIS). Unless otherwise stated p<0.05. Results At baseline, PBMCs from patients with SCD demonstrated elevated monocyte ROS generation and tissue factor expression than those from healthy controls. Inhibition of significantly reduced these measures of steady state monocyte activation. HSP90 inhibition also inhibited both LPS and cytokine induced tissue mRNA accumulation and subsequent cell surface expression of tissue factor in monocytes. Cytokine- induced ROS generation was significantly interrupted in monocytes upon inhibition of HSP90. A panel of monocyte pro-inflammatory genes could be inhibited with AUY922, whereas the anti-inflammatory cytokine, IL-10, was induced upon HSP90 inhibition with AUY922. Mechanistically, we also noted a profound translocation of NFkB to the monocyte nucleus upon cytokine stimulation. Consistent with the effects on tissue factor expression, pro-inflammatory potential, and ROS generation, this translocation could be completely ablated with HSP90 inhibition. Importantly, HSP90 inhibitors significantly attenuated the LPS-activated monocyte -induced lung microvascular endothelial permeability. Conclusion Our data suggest that Hsp90 inhibitors significantly reduced the both pro-inflammatory and pro-coagulatory potential of PBMCs from patients with SCD. These results thus position HSP90 as a potential master regulator of hemostasis, endothelial cell permeability, and thus suggest that HSP90 is an attractive therapeutic target in patients with SCD. Disclosures: Kutlar: Celgene Corporation: Research Funding. Meiler:Celgene Corporation: Research Funding.

scholarly journals Integral Role of RhoA Activation in Monocyte Adhesion–Triggered Tissue Factor Expression in Endothelial Cells

2003 ◽  
Vol 23 (4) ◽  
pp. 681-687 ◽  
Author(s):  
Toshiyuki Ishibashi ◽  
Takayuki Sakamoto ◽  
Hiroshi Ohkawara ◽  
Kenji Nagata ◽  
Koichi Sugimoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Tissue Factor Expression ◽  
Monocyte Adhesion ◽  
Rhoa Activation ◽  
Factor Expression ◽  
Integral Role

scholarly journals Activation of endothelial intrinsic NF-κB pathway impairs protein C anticoagulation mechanism and promotes coagulation in endotoxemic mice

Blood ◽  
2009 ◽  
Vol 114 (12) ◽  
pp. 2521-2529 ◽  
Author(s):  
Dongmei Song ◽  
Xiaobing Ye ◽  
Honglei Xu ◽  
Shu Fang Liu
Keyword(s):  
Transgenic Mice ◽  
Tissue Factor ◽  
Protein C ◽  
Nuclear Factor Κb ◽  
Tissue Factor Expression ◽  
Wild Type ◽  
Endothelial Protein C Receptor ◽  
Lps Challenge ◽  
Factor Expression

Abstract Although the role of systemic activation of the nuclear factor κB (NF-κB) pathway in septic coagulation has been well documented, little is known about the contribution of endothelial-specific NF-κB signaling in this pathologic process. Here, we used transgenic mice that conditionally overexpress a mutant I-κBα, an inhibitor of NF-κB, selectively on endothelium, and their wild-type littermates to define the role of endothelial-specific NF-κB in septic coagulation. In wild-type mice, lipopolysaccharide (LPS) challenge (5 mg/kg intraperitoneally) caused markedly increased plasma markers of coagulation, decreased plasma fibrinogen level, and widespread tissue fibrin deposition, which were abrogated by endothelial NF-κB blockade in transgenic mice. Endothelial NF-κB blockade inhibited tissue factor expression in endothelial cells, but not in leukocytes. Endothelial NF-κB blockade did not inhibit LPS-induced tissue factor expression in heart, kidney, and liver. Endothelial NF-κB blockade prevented LPS down-regulation of endothelial protein C receptor (EPCR) and thrombomodulin protein expressions, inhibited tissue tumor necrosis factor-α converting enzyme activity, reduced EPCR shedding, and restored plasma protein C level. Our data demonstrate that endothelial intrinsic NF-κB signaling plays a pivotal role in septic coagulation and suggests a link between endothelial-specific NF-κB activation and the impairment of the thrombomodulin-protein C-EPCR anticoagulation pathway.

Monocyte Adhesion and Transmigration Induce Tissue Factor Expression: Role of the Mitogen-Activated Protein Kinases

Shock ◽  
2002 ◽  
Vol 18 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Ian D. McGilvray ◽  
Vance Tsai ◽  
John C. Marshall ◽  
Alan P. B. Dackiw ◽  
Ori D. Rotstein
Keyword(s):  
Tissue Factor ◽  
Protein Kinases ◽  
Tissue Factor Expression ◽  
Monocyte Adhesion ◽  
Mitogen Activated Protein Kinases ◽  
Factor Expression ◽  
Mitogen Activated Protein

Role of monocyte-lineage cells in prostate cancer cell invasion and tissue factor expression

The Prostate ◽  
2010 ◽  
Vol 70 (15) ◽  
pp. 1672-1682 ◽  
Author(s):  
Paul F. Lindholm ◽  
Yi Lu ◽  
Brian P. Adley ◽  
Tudor Vladislav ◽  
Borko Jovanovic ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tissue Factor ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Prostate Cancer Cell ◽  
Tissue Factor Expression ◽  
Cancer Cell Invasion ◽  
Factor Expression
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