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Inhibition of platelet adhesion to collagen by monoclonal anti‐CD36 antibodies
Author(s) -
MATSUNO KAZUHIKO,
DIAZRICART MARIBEL,
MONTGOMERY ROBERT R.,
ASTER RICHARD H.,
JAMIESON G. A.,
TANDON NARENDRA N.
Publication year - 1996
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1996.422962.x
Subject(s) - monoclonal antibody , immunogen , cd36 , platelet , microbiology and biotechnology , chemistry , adhesion , antibody , flow cytometry , platelet activation , platelet adhesiveness , biochemistry , biology , immunology , receptor , platelet aggregation , organic chemistry
Monoclonal anti CD36 antibodies capable of inhibiting platelet adhesion to collagen have not previously been identified. We have now prepared two groups of monoclonal antibodies. One group was prepared using, as immunogen, highly purified (99+%) CD36 prepared by a denaturing procedure. These antibodies (Mo series) reacted strongly with CD36 on protein blots but did not immunoprecipitate native CD36 from platelet lysates nor inhibit platelet adhesion to collagen. The second group of monoclonal antibodies (131 series) was prepared using CD36 purified to >95% by a non‐denaturing procedure. These antibodies reacted with control platelets, but not Nak a ‐negative platelets which lack CD36, as measured by flow cytometry and by immunoprecipitation. Three monoclonal antibodies of this latter group (131.4, 131.5 and 131.7) inhibited platelet adhesion to collagen in static systems under Mg 2+ ‐independent conditions but had little effect in the presence of Mg 2+ . 131.4 and 131.7 also inhibited adhesion to collagen using citrated whole blood in a parallel plate flow chamber at physiological shear rates (800 s −1 ), whereas 131.5 was without effect. These are the first anti‐CD36 monoclonal antibodies shown to be capable of inhibiting platelet adhesion to collagen and provide further evidence that CD36 plays a role in platelet–collagen interaction.