Sulfated glycoconjugates enhance CD36-dependent adhesion ofPlasmodium falciparum–infected erythrocytes to human microvascular endothelial cells

Blood ◽  
2000 ◽  
Vol 96 (1) ◽  
pp. 327-333 ◽  
Author(s):  
Christopher John McCormick ◽  
Christopher I. Newbold ◽  
Anthony R. Berendt
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Dextran Sulfate ◽  
Umbilical Vein ◽  
Microvascular Endothelial Cells ◽  
Cos Cells ◽  
Ofplasmodium Falciparum ◽  
Microvascular Endothelial ◽  
Umbilical Vein Endothelial Cells ◽  
Negative Cell Line

Abstract A novel adhesive pathway that enhances the adhesion ofPlasmodium falciparum-infected erythrocytes (IEs) to endothelial cells has been identified. The sulfated glycoconjugates heparin, fucoidan, dextran sulfate 5000, and dextran sulfate 500 000 caused a dramatic increase in adhesion of IEs to human dermal microvascular endothelial cells. The same sulfated glycoconjugates had little effect on IE adhesion to human umbilical vein endothelial cells, a CD36-negative cell line. The effect was abolished by a monoclonal antibody directed against CD36, suggesting that enhanced adhesion to endothelium is dependent on CD36. No effect was observed on adhesion to purified platelet CD36 cells immobilized on plastic. The same sulfated glycoconjugates enhanced adhesion of infected erythrocytes to COS cells transfected with CD36, and this was inhibited by the CD36 monoclonal antibody. These findings demonstrate a role for sulfated glycoconjugates in endothelial adherence that may be important in determining the location and magnitude of sequestration through endogenous carbohydrates. In addition, they highlight possible difficulties that may be encountered from the proposed use of sulfated glycoconjugates as antiadhesive agents in patients with severe malaria.

Sulfated glycoconjugates enhance CD36-dependent adhesion ofPlasmodium falciparum–infected erythrocytes to human microvascular endothelial cells

Blood ◽  
2000 ◽  
Vol 96 (1) ◽  
pp. 327-333 ◽  
Author(s):  
Christopher John McCormick ◽  
Christopher I. Newbold ◽  
Anthony R. Berendt
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Dextran Sulfate ◽  
Umbilical Vein ◽  
Microvascular Endothelial Cells ◽  
Cos Cells ◽  
Ofplasmodium Falciparum ◽  
Microvascular Endothelial ◽  
Umbilical Vein Endothelial Cells ◽  
Negative Cell Line

A novel adhesive pathway that enhances the adhesion ofPlasmodium falciparum-infected erythrocytes (IEs) to endothelial cells has been identified. The sulfated glycoconjugates heparin, fucoidan, dextran sulfate 5000, and dextran sulfate 500 000 caused a dramatic increase in adhesion of IEs to human dermal microvascular endothelial cells. The same sulfated glycoconjugates had little effect on IE adhesion to human umbilical vein endothelial cells, a CD36-negative cell line. The effect was abolished by a monoclonal antibody directed against CD36, suggesting that enhanced adhesion to endothelium is dependent on CD36. No effect was observed on adhesion to purified platelet CD36 cells immobilized on plastic. The same sulfated glycoconjugates enhanced adhesion of infected erythrocytes to COS cells transfected with CD36, and this was inhibited by the CD36 monoclonal antibody. These findings demonstrate a role for sulfated glycoconjugates in endothelial adherence that may be important in determining the location and magnitude of sequestration through endogenous carbohydrates. In addition, they highlight possible difficulties that may be encountered from the proposed use of sulfated glycoconjugates as antiadhesive agents in patients with severe malaria.

Clot Lysis Mediated by Cultured Human Microvascular Endothelial Cells

1988 ◽  
Vol 60 (03) ◽  
pp. 463-467 ◽  
Author(s):  
Wolfgang Speiser ◽  
Elisabeth Anders ◽  
Bernd R Binder ◽  
Gert Müller-Berghaus
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Shape Change ◽  
Umbilical Vein ◽  
Cell Types ◽  
Microvascular Endothelial Cells ◽  
Clot Lysis ◽  
Microvascular Endothelial ◽  
Umbilical Vein Endothelial Cells ◽  
Fibrin Clots

SummaryThe lysis of fibrin clots on the surface of cultured human omental tissue microvascular endothelial cells (HOTMEC) and cultured human umbilical vein endothelial cells (HUVEC) was studied. Fibrin clots were made by mixing fibrinogen, plasminogen and thrombin on the surface of both cell types. Clot lysis was seen only on the surface of HOTMEC, which were found to synthesize about 100-fold more tissue plasminogen activator (tPA) antigen than HUVEC. Clot lysis of HOTMEC could be blocked by anti-tPA IgG but was not affected by the incorporation of exogenous plasminogen activator (PAI) into the clot in concentrations (75 arbitrary units) exceeding the tPA activity (21 ± 2.5 IU) of the cells. Thus, it is likely that tPA secreted by HOTMEC is protected from inhibition by PAI in the presence of fibrin and endothelial cells. The stimulation of EC to release an excess of tPA over PAI, in contrast to the secretion of an excess of PAI over tPA found in unstimulated cells in the absence of fibrin, is obviously no prerequisite for the initiation of fibrinolysis on the surface of HOTMEC. As thrombin was used for clot formation, its influence on tPA and PAI synthesis of both cell types was investigated. In contrast to HOTMEC, which were not affected by Α-thrombin, HUVEC revealed a dose-dependent increase in tPA and PAI synthesis upon incubation with the enzyme. This increase in tPA production by HUVEC was not sufficient to lyse the clots within 48 hours. Furthermore, HUVEC. behaved differently towards thrombin as these cells in contrast to HOTMEC revealed the typical shape change reaction upon incubation with the enzyme

scholarly journals Rapid Secretion of Prestored Interleukin 8 from Weibel-Palade Bodies of Microvascular Endothelial Cells

1998 ◽  
Vol 188 (9) ◽  
pp. 1751-1756 ◽  
Author(s):  
Jon Olav Utgaard ◽  
Frode L. Jahnsen ◽  
Arne Bakka ◽  
Per Brandtzaeg ◽  
Guttorm Haraldsen
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Microvascular Endothelial Cells ◽  
Double Positive ◽  
Endothelial Cell Surface ◽  
Microvascular Endothelial ◽  
Umbilical Vein Endothelial Cells ◽  
Von Willebrand ◽  
Umbilical Cords ◽  
Willebrand Factor

Interleukin (IL)-8, a C-X-C chemokine, activates integrin-mediated adhesion of neutrophils. Presentation of IL-8 on the endothelial cell surface may promote leukocyte extravasation. We found that cultured human microvascular endothelial cells from the intestine (HIMEC) and from nasal polyps (PMEC), but not human umbilical vein endothelial cells (HUVEC), contained IL-8 in intracellular granules that coexpressed von Willebrand factor (vWf  ). This observation was corroborated by the immunohistochemical observation of double-positive granules (IL-8+vWf+) in vessels of small and large intestine, nasal mucosa, and skin, whereas umbilical cords revealed no endothelial IL-8. After treatment of HIMEC or PMEC with histamine or thrombin, a dramatic increase in supernatant IL-8 concentration was observed within 3 min, whereas no increase in IL-8 was detected in supernatants of identically treated HUVEC cultures. Histamine or thrombin treatment also caused IL-8–containing granules to rapidly disappear from HIMEC. In HUVEC, IL-8–containing granules were inducible by treatment with recombinant human IL-1β for 24 h; additional histamine treatment doubled IL-8 secretion from HUVEC in the same rapid manner observed for mucosal EC. These data suggested that IL-8 prestored in microvascular endothelial cells may provide a rapid pathway for specific activation of neutrophil adhesion at sites of acute inflammation.

scholarly journals Verocytotoxin-Induced Apoptosis of Human Microvascular Endothelial Cells

2001 ◽  
Vol 12 (4) ◽  
pp. 767-778
Author(s):  
ANTONETTA H. J. M. PIJPERS ◽  
PETRA A. VAN SETTEN ◽  
LAMBERTUS P. W. J. VAN DEN HEUVEL ◽  
KAREL J. M. ASSMANN ◽  
HENDRIKUS B. P. M. DIJKMAN ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Protein Synthesis ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Microvascular Endothelial Cells ◽  
Tnf Α ◽  
Microvascular Endothelial ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Abstract. The pathogenesis of the epidemic form of hemolytic uremic syndrome is characterized by endothelial cell damage. In this study, the role of apoptosis in verocytotoxin (VT)-mediated endothelial cell death in human glomerular microvascular endothelial cells (GMVEC), human umbilical vein endothelial cells, and foreskin microvascular endothelial cells (FMVEC) was investigated. VT induced apoptosis in GMVEC and human umbilical vein endothelial cells when the cells were prestimulated with the inflammatory mediator tumor necrosis factor-α (TNF-α). FMVEC displayed strong binding of VT and high susceptibility to VT under basal conditions, which made them suitable for the study of VT-induced apoptosis without TNF-α interference. On the basis of functional (flow cytometry and immunofluorescence microscopy using FITC-conjugated annexin V and propidium iodide), morphologic (transmission electron microscopy), and molecular (agarose gel electrophoresis of cellular DNA fragments) criteria, it was documented that VT induced programmed cell death in microvascular endothelial cells in a dose- and time-dependent manner. Furthermore, whereas partial inhibition of protein synthesis by VT was associated with a considerable number of apoptotic cells, comparable inhibition of protein synthesis by cycloheximide was not. This suggests that additional pathways, independent of protein synthesis inhibition, may be involved in VT-mediated apoptosis in microvascular endothelial cells. Specific inhibition of caspases by Ac-Asp-Glu-Val-Asp-CHO, but not by Ac-Tyr-Val-Ala-Asp-CHO, was accompanied by inhibition of VT-induced apoptosis in FMVEC and TNF-α-treated GMVEC. These data indicate that VT can induce apoptosis in human microvascular endothelial cells.

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