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(1–3)Gal Binding Lectin: Up-Regulation of CD59 Expression1
Departments of Surgery and Laboratory Medicine and Pathology, School of Medicine, and Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, and Department of Veterans Affairs Medical Center, Minneapolis, MN 55417
Endothelial cells (EC) play central roles in vascular physiology
and pathophysiology. EC activation results in proinflammatory
activities with production of cytokines and expression of adhesion
molecules. However, we have shown before in a model of
xenotransplantation that prolonged stimulation of porcine EC with human
anti-porcine IgM natural Abs can activate the cells to become
resistant against cytotoxicity by the membrane attack complex of
complement (MAC). Now we report the major characteristics of induction
and maintenance of resistance elicited in porcine EC with
Bandeiraea simplicifolia lectin that binds terminal
gal
(1–3)gal. Lectin-treated cells underwent little or no
cytotoxicity and PGI2 release when exposed to MAC.
Induction of resistance required incubation of the EC with lectin for
4 h but was not fully manifested until 16 h later. Most of
the initially bound lectin remained on the cell surface for >60 h.
EC-bound lectin did not inhibit binding of IgM natural Abs or
activation and binding of C components, including C9, but a C-induced
permeability channel of reduced size was present. Induction of
resistance required protein synthesis, developed slowly, and was
associated with up-regulation of expression of mRNA for the MAC
inhibitor CD59 and membrane-associated CD59 protein. Resistance lasted
at least 3 days, and the cells regained normal morphology and were
metabolically active. This induced resistance may have a physiologic
counterpart that might be amenable to pharmacologic manipulation in
vascular endothelium pathophysiology.
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