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Membrane glycoproteins and platelet cytoskeleton in immune complex- induced
platelet activation
J Kang, C Cabral, L Kushner and EW Salzman
Department of Surgery, Beth Israel Hospital, Harvard Medical School,
Boston, MA 02215.
To clarify the mechanism of platelet activation by immune complexes and the
possible involvement of surface glycoproteins (GPs), we studied platelet
activation induced by heat-aggregated IgG (HAG). We examined the effects of
monoclonal antibodies (MoAbs) against GPIb, GPIIb/IIIa, and the Fc receptor
on resting platelets and on platelets stimulated by HAG. HAG increased the
cytosolic ionized calcium concentration ([Ca2+]i) and stimulated protein
(P47 and P20) phosphorylation, phosphatidic acid (PA) synthesis, serotonin
secretion, and platelet aggregation. IV.3, an anti-Fc gamma RII receptor
MoAb, inhibited HAG binding to platelets and all subsequent platelet
responses. Like IV.3, MoAbs against GPIIb/IIIa (Tab, 10E5, AP-3) or GPIb
(AP-1, 6D1) strongly inhibited platelet activation by HAG. However, while
anti-GPIIb/IIIa MoAbs inhibited binding of IV.3 and HAG to platelets,
anti-GPIb MoAbs had little effect on platelet binding of IV.3 or HAG. These
observations suggest a close topographical and functional association of
GPIIb/IIIa with Fc gamma RII in the platelet response to HAG. Cytochalasin
B, an inhibitor of actin polymerization, also inhibited platelet activation
but not HAG or IV.3 binding. Measurement of the fluorescence of
7-nitrobenz-2-oxa-1,3-(NBD)-phallacidin, a specific marker for filamentous
actin (F-actin), showed that both cytochalasin B and AP-1 blocked the
increase of F-actin induced by HAG. The common effects of anti-GPIb MoAbs
and of cytochalasin B suggest that unlike the activity of GPIIb/IIIa, the
ability of anti-GPIb to inhibit the activation of platelets by immune
complexes is associated with perturbation of the cytoskeleton.
Volume 81,
Issue 6,
pp. 1505-1512,
03/15/1993
Copyright © 1993 by The American Society of Hematology
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