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THE EFFECT OF VARIOUS FORMS OF HEPARIN ON THE RELEASE OF IMMUNE COMPLEXES FROM THE SURFACE OF CULTURED MESANGIAL CELLS
Author(s) -
DRAKELEY SIMON J.,
FURNESS PETER N.
Publication year - 1996
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199604)178:4<458::aid-path500>3.0.co;2-e
Subject(s) - heparin , immune system , mesangial cell , immune complex , in vivo , chemistry , in vitro , microbiology and biotechnology , biochemistry , biophysics , biology , immunology
Heparin is capable of enhancing the rate of release of antigen from nephritic rat kidneys. It also interferes with the binding of immune complexes by cultured glomerular mesangial cells. Postulating that these two effects might be related, we sought to determine what basic aspects of the molecular structure of heparin are responsible for the interference with binding in vitro . After cultured mesangial cells had bound radiolabelled synthetic immune complexes, heparin or a variety of structurally related molecules were added to the supernatant. De‐N‐sulphated heparin, heparan sulphate, low molecular weight heparin, and low molecular weight dextran sulphate had no effect on immune complex binding. High molecular weight dextran sulphate was able, like heparin, to dislodge immune complexes from mesangial cells, suggesting that high molecular weight and high sulphation are required. These results differ from previous findings in vivo , suggesting that the effect of heparin in vivo is not due to interaction at the mesangial cell surface. Alternative explanations for the effect of heparin in the intact animal include destabilization of the immune complex structure or, more probably, an effect at the boundary between the immune complex deposit and the basement membrane.