scholarly journals Differential expression of Toll-like receptor 2 (TLR2) and responses to TLR2 ligands between human and murine vascular endothelial cells

2007 ◽  
Vol 13 (5) ◽  
pp. 281-296 ◽  
Author(s):  
Shuang Chen ◽  
Michelle H. Wong ◽  
Danica J. Schulte ◽  
Moshe Arditi ◽  
Kathrin S. Michelsen
Keyword(s):  
Endothelial Cells ◽  
Differential Expression ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Tlr2 Ligands

Differential expression of the two VEGF receptors flt and KDR in placenta and vascular endothelial cells

1994 ◽  
Vol 54 (1) ◽  
pp. 56-66 ◽  
Author(s):  
Bernhard Barleon ◽  
Stefanie Hauser ◽  
Claudia Schöllmann ◽  
Karin Weindel ◽  
Dieter Marmé ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Differential Expression ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Vegf Receptors

scholarly journals Absence of TRAM Restricts Toll-Like Receptor 4 Signaling in Vascular Endothelial Cells to the MyD88 Pathway

2006 ◽  
Vol 98 (9) ◽  
pp. 1134-1140 ◽  
Author(s):  
Olivier A. Harari ◽  
Pilar Alcaide ◽  
Daniela Ahl ◽  
F. William Luscinskas ◽  
James K. Liao
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Myd88 Pathway

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

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