scholarly journals A Novel Zinc Finger Protein mRNA in Human Umbilical Vein Endothelial Cells is Profoundly Induced by Tumor Necrosis Factor ^|^alpha;

2000 ◽  
Vol 7 (2) ◽  
pp. 97-103 ◽  
Author(s):  
Chikage Mataki ◽  
Takeshi Murakami ◽  
Michihisa Umetani ◽  
Youichiro Wada ◽  
Masami Ishii ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Zinc Finger Protein ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Finger Protein ◽  
Factor Alpha ◽  
Umbilical Vein Endothelial Cells ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor Alpha Increases Human Cerebral Endothelial Cell Gb3 and Sensitivity to Shiga Toxin

2001 ◽  
Vol 69 (3) ◽  
pp. 1889-1894 ◽  
Author(s):  
Patricia B. Eisenhauer ◽  
Prasoon Chaturvedi ◽  
Richard E. Fine ◽  
Andrew J. Ritchie ◽  
Jordan S. Pober ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Umbilical Vein ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Hemolytic uremic syndrome (HUS) is associated with intestinal infection by enterohemorrhagic Escherichia coli strains that produce Shiga toxins. Globotriaosylceramide (Gb3) is the functional receptor for Shiga toxin, and tumor necrosis factor alpha (TNF-α) upregulates Gb3 in both human macrovascular umbilical vein endothelial cells and human microvascular brain endothelial cells. TNF-α treatment enhanced Shiga toxin binding and sensitivity to toxin. This upregulation was specific for Gb3 species containing normal fatty acids (NFA). Central nervous system (CNS) pathology in HUS could involve cytokine-stimulated elevation of endothelial NFA-Gb3 levels. Differential expression of Gb3 species may be a critical determinant of Shiga toxin toxicity and of CNS involvement in HUS.

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