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J. Biol. Chem., Vol. 268, Issue 21, 15484-15488, Jul, 1993
TG Obrig, CB Louise, CA Lingwood, B Boyd, L Barley-Maloney and TO Daniel
This study addresses the basis for regional microvascular susceptibility to
bacterial toxins implicated in hemolytic uremic syndrome. The results
indicate a relationship between the degree of Shiga toxin sensitivity of
human endothelial cells from different sources and the amount of
globotriaosylceramide (Gb3) glycosphingolipid receptor for Shiga toxin
expressed by these cells. Cell viability and protein synthesis of renal
endothelial cells were reduced to 50% by 1 pM Shiga toxin, while umbilical
vein cells were not affected by > 1 nM toxin. Similarly, basal levels of
Gb3 were approximately 50 times higher in renal endothelial cells than in
the umbilical endothelial cells. Pre-exposure of umbilical endothelial
cells to tumor necrosis factor-alpha or bacterial lipopolysaccharide
increased Gb3 content 4-6- fold coincident with increases in sensitivity to
cytotoxic and protein synthesis inhibitory effects of Shiga toxin.
Lipopolysaccharide induction of both Gb3 and sensitivity to Shiga toxin
cytotoxic action in umbilical endothelial cells was dependent on the
structure of lipopolysaccharide. Neither tumor necrosis factor-alpha nor
lipopolysaccharide altered the Shiga toxin sensitivity or the Gb3 content
of renal endothelial cells. These data indicate that differential
endothelial expression of glycolipid receptors for Shiga toxins may be
responsible for localized involvement of the kidney in hemolytic uremic
syndrome.
Endothelial heterogeneity in Shiga toxin receptors and responses
Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, New York 14642.
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