Release of heparan sulfate from endothelial cells: implications for pathogenesis of hyperacute rejection

Heparan sulfate proteoglycan associated with endothelial cells in normal blood vessels inhibits intravascular coagulation and egress of blood cells and plasma proteins, key features of hyperacute rejection. It was shown herein that exposure of cultured porcine endothelium to human serum as a source...

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Published inThe Journal of experimental medicine Vol. 171; no. 4; pp. 1363 - 1368
Main Authors PLATT, J. L, VERCELLOTTI, G. M, LINDMAN, B. J, OEGEMA, T. R. JR, BACH, F. H, DALMASSO, A. P
Format Journal Article
LanguageEnglish
Published New York, NY Rockefeller University Press 01.04.1990
The Rockefeller University Press
Subjects
Analysis of the immune response. Humoral and cellular immunity
Animals
Aorta
Biological and medical sciences
Blood Physiological Phenomena
Cells, Cultured
Endothelium, Vascular - immunology
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Glycosaminoglycans - metabolism
Graft Rejection
Heparitin Sulfate - metabolism
Humans
Immunobiology
Kinetics
Models, Biological
Organs and cells involved in the immune response
Proteoglycans - isolation & purification
Sulfates - metabolism
Sulfur Radioisotopes
Swine
Cell culture
Endothelial cell
Radiolabelling
Antibody
Cytotoxicity
Complement
Pig
Vertebrata
Mammalia
Electrophoresis
Glycosaminoglycan
Heparitin sulfate
Serum
Artiodactyla
Ungulata
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Summary:Heparan sulfate proteoglycan associated with endothelial cells in normal blood vessels inhibits intravascular coagulation and egress of blood cells and plasma proteins, key features of hyperacute rejection. It was shown herein that exposure of cultured porcine endothelium to human serum as a source of natural antibodies and complement caused cleavage and release of 5% of endothelial cell proteoglycans within 4 min and greater than 50% within 1 h. Proteoglycan release depended on activation of the classical complement pathway and preceded irreversible cell injury. These findings suggest that loss of endothelial cell proteoglycan may be a critical step in the pathogenesis of hyperacute rejection and in diseases involving humoral injury to endothelial cells.
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ISSN:0022-1007
1540-9538
DOI:10.1084/jem.171.4.1363