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Activation of human platelets by the rabbit anticardiolipin antibodies
YL Lin and CT Wang
Institute of Life Science, National Tsing Hua University, Hsinchu, Taiwan.
Affinity purified anticardiolipin antibodies (ACLA) raised in rabbits
showed cross-reactivities with various negatively charged phospholipids as
shown by both the solid phase enzyme-linked immunosorbent assay (ELISA) and
inhibition studies. In ELISA, ACLA showed strong cross- reactivity to both
sphingomyelin (SM) and phosphatidylethanolamine (PE), but the inhibition
studies showed that ACLA failed to bind the aqueous suspensions of SM, PE,
and PE/PC (1:1). ACLA bound to resting gel-filtered human platelets (GFP)
as shown by both inhibition study and flow cytofluorometric analysis.
Western blotting procedure showed that ACLA strongly cross-reacted to an
80-Kd plasma membrane protein. ACLA activated platelet response in a
concentration-dependent manner. At less than 10 micrograms/mL, ACLA induced
both platelet shape change to spiculate irregular forms as shown by
scanning electron microscopy and the phosphorylation of 20-Kd protein. ACLA
at more than 10 micrograms/mL caused platelet aggregation and secretion.
The aggregation was inhibited by EDTA; aspirin; antimycin A plus 2-
deoxyglucose; PGE1; and the F(ab')2 fragment of ACLA. It was not inhibited
by monoclonal antibody to Fc receptor (MoAb FcR2). The biochemical events
of ACLA-induced platelet response involved the elevation of (1) thromboxane
A2 formation, (2) cytosolic free calcium ion concentration ([Ca2+]i), and
(3) 47-Kd protein phosphorylation. In addition, the subaggregatory
concentration of ACLA showed synergistic platelet activation with that
concentration of thrombin, collagen, and epinephrine. The study showed the
mechanism involved in ACLA-induced platelet responses.
Volume 80,
Issue 12,
pp. 3135-3143,
12/15/1992
Copyright © 1992 by The American Society of Hematology
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