Monoclonal Antibodies to Vascular Endothelial Cells - A Possible Tool for Detecting Endothelial Damage

1985 ◽  
Vol 69 (s12) ◽  
pp. 80P-80P
Author(s):  
D.P. de Bono ◽  
S. Pringle
Keyword(s):  
Endothelial Cells ◽  
Monoclonal Antibodies ◽  
Vascular Endothelial Cells ◽  
Endothelial Damage ◽  
Vascular Endothelial

Production of two novel monoclonal antibodies that distinguish mouse lymphatic and blood vascular endothelial cells

2006 ◽  
Vol 211 (5) ◽  
pp. 379-393 ◽  
Author(s):  
Taichi Ezaki ◽  
Kazuhiko Kuwahara ◽  
Shunichi Morikawa ◽  
Kazuhiko Shimizu ◽  
Nobuo Sakaguchi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Monoclonal Antibodies ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

Lectins as markers of endothelial cells: comparative study between human and animal cells

1988 ◽  
Vol 22 (2) ◽  
pp. 135-140 ◽  
Author(s):  
F. Roussel ◽  
J. Dalion
Keyword(s):  
Endothelial Cells ◽  
Monoclonal Antibodies ◽  
Comparative Study ◽  
Vascular Endothelial Cells ◽  
Human Cells ◽  
Point Of View ◽  
Laboratory Animals ◽  
Vascular Endothelial ◽  
Animal Cells ◽  
Common Laboratory

Vascular endothelial cells were labelled with 10 vegetal lectins and 3 more monoclonal antibodies antiblood group ABO substances, in major organs of 14 common laboratory animals. After fixation in PLPa and paraffin embedding, cells were examined to determine their likeness to human cells. The most interesting reactive used was EEA, whose positivity defines upper mammalians. Blood B substance positivity and CSA negativity defines primates among which man is unique and defined by UEA I positivity and variability in ABO substance. CSA positivity defines non-primate upper mammalians. Rodents and birds were negative with all reactives tested. From the histochemical point of view, the animals closest to humans are monkeys, followed by swine and oxen, then by cat and dog and lastly by sheep. Rodents appear unrelated to humans in this system.

scholarly journals Clostridium perfringens Epsilon-Toxin Increases Permeability of Single Perfused Microvessels of Rat Mesentery

2005 ◽  
Vol 73 (8) ◽  
pp. 4879-4887 ◽  
Author(s):  
R. H. Adamson ◽  
J. C. Ly ◽  
M. Fernandez-Miyakawa ◽  
S. Ochi ◽  
J. Sakurai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Clostridium Perfringens ◽  
Vascular Endothelial Cells ◽  
Intestinal Barrier ◽  
Endothelial Damage ◽  
Direct Access ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Rat Mesentery ◽  
Epsilon Toxin

ABSTRACT Epsilon-toxin, the primary virulence factor of Clostridium perfringens type D, causes mortality in livestock, particularly sheep and goats, in which it induces an often-fatal enterotoxemia. It is believed to compromise the intestinal barrier and then enter the gut vasculature, from which it is carried systemically, causing widespread vascular endothelial damage and edema. Here we used single perfused venular microvessels in rat mesentery, which enabled direct observation of permeability properties of the in situ vascular wall during exposure to toxin. We determined the hydraulic conductivity (Lp ) of microvessels as a measure of the response to epsilon-toxin. We found that microvessels were highly sensitive to toxin. At 10 μg ml−1 the Lp increased irreversibly to more than 15 times the control value by 10 min. At 0.3 μg ml−1 no increase in Lp was observed for up to 90 min. The toxin-induced increase in Lp was consistent with changes in ultrastructure of microvessels exposed to the toxin. Those microvessels exhibited gaps either between or through endothelial cells where perfusate had direct access to the basement membrane. Many endothelial cells appeared necrotic, highly attenuated, and with dense cytoplasm. We showed that epsilon-toxin, in a time- and dose-dependent manner, rapidly and irreversibly compromised the barrier function of venular microvessel endothelium. The results conformed to the hypothesis that epsilon-toxin interacts with vascular endothelial cells and increases the vessel wall permeability by direct damage of the endothelium.

scholarly journals Binding studies of anti-human platelet glycoprotein IIb/IIIa monoclonal antibodies to cultured vascular endothelial cells.

1987 ◽  
Vol 18 (3) ◽  
pp. 239-242
Author(s):  
Tokuo NAKAJIMA ◽  
Yoshio OURA ◽  
Reiko UESHIMA ◽  
Hiroko TANAKA ◽  
Tetsuji KOYAMA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Monoclonal Antibodies ◽  
Vascular Endothelial Cells ◽  
Human Platelet ◽  
Platelet Glycoprotein ◽  
Vascular Endothelial ◽  
Binding Studies

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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