Abstract 337: Plasma Advanced-oxidized Protein Products Promote Platelet-endothelial Crosstalk and Endothelial Tissue Factor Expression

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Lisa Pasterk ◽  
Sandra Lemesch ◽  
Bettina Leber ◽  
Markus Trieb ◽  
Sanja Curcic ◽  
...  
Keyword(s):  
Renal Disease ◽  
Tissue Factor ◽  
Platelet Activation ◽  
Platelet Reactivity ◽  
Tissue Factor Expression ◽  
Serum Samples ◽  
Platelet Aggregometry ◽  
Factor Expression ◽  
Esrd Patients

Background/Aims: End-stage renal disease (ESRD) is associated with a prothrombotic phenotype and substantial activation of platelets can occur in the course of hemodialysis. However, the underlying mechanisms for increased platelet reactivity remain unclear. Increased levels of oxidized albumin, termed “advanced oxidation protein products (AOPPs)” accumulate in subjects with renal disease. Methods: Platelet aggregation was assessed with platelet aggregometry. Platelet activation, formation of reactive oxygen species and tissue factor expression on the surface of platelets and endothelial cells was measured by flow cytometry. Platelet adherence was assessed under flow using the Cellix system. The oxidative status of albumin isolated from ESRD patients was determined by photometric analysis. Tissue factor levels in serum samples were determined using a commercially available ELISA kit. Results: Albumin isolated from hemodialysis patients as well as in vitro generated AOPP-albumin promoted platelet activation via CD36, dependent on the AOPP-content of albumin. AOPP-albumin mediated platelet activation was prevented by scavenging superoxide anions and inhibitors of phospholipase C and protein kinase C. Furthermore, AOPP and serum tissue factor levels were considerably increased in ESRD patients on hemodialysis and a significant correlation of AOPP and serum tissue factor was found. Conclusion: Interaction of platelet CD36 with endogenous oxidized albumin may link oxidative stress with a prothrombotic phenotype in ESRD.

Upregulation of tissue factor expression by avastin: ex vivo and in vitro data

2012 ◽  
Vol 129 ◽  
pp. S170
Author(s):  
E. Napoleone ◽  
A. Cutrone ◽  
D. Cugino ◽  
R. Tambaro ◽  
A. De Curtis ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Ex Vivo ◽  
Tissue Factor Expression ◽  
Factor Expression ◽  
Vitro Data ◽  
In Vitro Data

Nutritional compounds influence tissue factor expression and inflammation of chronic kidney disease patients in vitro

Nutrition ◽  
2011 ◽  
Vol 27 (9) ◽  
pp. 967-972 ◽  
Author(s):  
Cecilia M. Shing ◽  
Murray J. Adams ◽  
Robert G. Fassett ◽  
Jeff S. Coombes
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Tissue Factor ◽  
Tissue Factor Expression ◽  
Factor Expression ◽  
Nutritional Compounds

scholarly journals Dietary α-Linolenic Acid Inhibits Arterial Thrombus Formation, Tissue Factor Expression, and Platelet Activation

2011 ◽  
Vol 31 (8) ◽  
pp. 1772-1780 ◽  
Author(s):  
Erik W. Holy ◽  
Marc Forestier ◽  
Eva K. Richter ◽  
Alexander Akhmedov ◽  
Florian Leiber ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Linolenic Acid ◽  
Platelet Activation ◽  
Thrombus Formation ◽  
Tissue Factor Expression ◽  
Arterial Thrombus ◽  
Factor Expression

scholarly journals Vascular Gas6 contributes to thrombogenesis and promotes tissue factor up-regulation after vessel injury in mice

Blood ◽  
2013 ◽  
Vol 121 (4) ◽  
pp. 692-699 ◽  
Author(s):  
Richard S. Robins ◽  
Catherine A. Lemarié ◽  
Sandrine Laurance ◽  
Meghedi N. Aghourian ◽  
Jianqiu Wu ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Thrombus Formation ◽  
Vascular Wall ◽  
Specific Gene ◽  
Tissue Factor Expression ◽  
Vessel Injury ◽  
Factor Expression ◽  
Platelet Signaling

Abstract Gas6 (growth-arrest specific gene 6) plays a role in thrombus stabilization. Gas6 null (−/−) mice are protected from lethal venous and arterial thromboembolism through platelet signaling defects induced only by 5μM ADP and 10μM of the thromboxane analog, U46619. This subtle platelet defect, despite a dramatic clinical phenotype, raises the possibility that Gas6 from a source other than platelets contributes to thrombus formation. Thus, we hypothesize that Gas6 derived from the vascular wall plays a role in venous thrombus formation. Bone marrow transplantation and platelet depletion/reconstitution experiments generating mice with selective ablations of Gas6 from either the hematopoietic or nonhematopoietic compartments demonstrate an approximately equal contribution by Gas6 from both compartments to thrombus formation. Tissue factor expression was significantly reduced in the vascular wall of Gas6−/− mice compared with WT. In vitro, thrombin-induced tissue factor expression was reduced in Gas6−/− endothelial cells compared with wild-type endothelium. Taken together, these results demonstrate that vascular Gas6 contributes to thrombus formation in vivo and can be explained by the ability of Gas6 to promote tissue factor expression and activity. These findings support the notion that vascular wall-derived Gas6 may play a pathophysiologic role in venous thromboembolism.

P-043 Preeclampsia: Platelet activation, platelet-leukocyte aggregates and tissue factor expression assessment

2013 ◽  
Vol 131 ◽  
pp. S88
Author(s):  
L.G. Freitas ◽  
M.G. Carvalho ◽  
O.A. Martins-Filho ◽  
R. Sathler-Avelar ◽  
L.M.S. Dusse
Keyword(s):  
Tissue Factor ◽  
Platelet Activation ◽  
Tissue Factor Expression ◽  
Factor Expression

Platelet activation and increased tissue factor expression on monocytes in reperfusion injury following orthotopic liver transplantation

Platelets ◽  
2010 ◽  
Vol 21 (5) ◽  
pp. 348-359 ◽  
Author(s):  
Jan Schulte Am Esch ◽  
Kerstin Jurk ◽  
Wolfram T. Knoefel ◽  
Gesine Roeder ◽  
Holger Voss ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Reperfusion Injury ◽  
Tissue Factor ◽  
Orthotopic Liver Transplantation ◽  
Platelet Activation ◽  
Tissue Factor Expression ◽  
Factor Expression
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