Receptor–ligand complexes are cleared to the open canalicular system of surface‐activated platelets

Abstract

Human platelets were incubated with gold particles coupled to fibrinogen to label the glycoprotein IIb-IIIa (GPIIb-IIIa) receptor after initial activation of the cells by contact with formvar-coated grid and glass surfaces. Fibrinogen-gold (Fgn-Au) markers were absent on discoid platelets, but diffusely spread over the surface and extended pseudopods of early dendritic cells. Conversion to spread platelets resulted in movement of ligand-receptor complexes away from the cell margin toward cell centres. However, Fgn-Au gold did not concentrate in the central region. Rather, the Fgn-Au, GPIIb-IIIa complexes in the middle of spread platelets appeared to move toward a belt-like, intermediate zone, as did the ligand receptor complexes from the cell margin and pseudopods. The ultimate destination of the mobile receptor-ligand complexes, however, appeared to be channels of the surface-connected open canalicular system (OCS). Fgn-Au was concentrated in OCS channels of most dendritic and a small proportion of spread platelets. The decreased frequency of Fgn-Au filled channels in more transformed platelets may have been due to collapse or evagination of the OCS. Examination of platelets exposed to Fgn-Au after spreading on glass and then prepared for thin sections confirmed that the OCS was the final destination for mobile ligand receptor complexes on surface-activated platelets. Findings of this study are consistent with previous work showing clearance of mobile receptor-ligand complexes to the OCS of platelets activated in suspension.

Blood Platelets Are Circulating Stores for Adhesive Proteins, Inflammatory Mediators, and Immunoglobulins – Role in Nonhemolytic Transfusion Reactions

“…3b). The biological meaning of this activation-dependent translocation of FcγRII into the OCS is so far not clear, but several glycoproteins (GP Ibα, GP V, GP IX) share this common mechanism and are assumed to regulate the platelets' interactions with surfaces and other cells in this way [39,40]. The close association between the IgE receptor CD 23 and the GP IIb/IIIa complex [41] is an example for the formation of large protein complexes in the platelet membrane, and it is tempting to speculate on a comparable mechanism underlying the redistribution of FcγRII.…”

EDTA induced changes in platelet structure and function: influence on particle uptake

“…stored at -70°C and then thawed prior to absorption. Colloidal gold particles having a diameter of 16 -18 nm were coated with fibrinogen in the manner described by Loftus and Albrecht, 1 2 by Leistikow et al, 8 and by Escolar et al 1 3 Uncoated colloidal gold particles were also used in each experiment.…”

“…The reduced diameter of 'zippered' OCS channels and dissociation of GPIIb/IIIa m ay prevent translocation and clearance of particulates and receptorligand com plexes. 8 The present study has evaluated the interaction of EDTA-treated platelets with particulates in suspension. Results indicate that some of the functional responses of EDTA platelets are not irreversibly compromised by exposure to the chelating agent.…”

Ultrastructure of platelets and platelet-surface interactions

“…A series of recent investigations have used formvar films to investigate the organization of fibrinogen receptor after surface activation of human platelets [26][27][28][29]. The abluminal or ventral side with which platelets relate to the substrata and the luminal or dorsal side that provides a relation of the attached platelet with other platelets or cell elements.…”

“…This initial work emphasized the fact that Fgn-Au complexes were moved from peripheral margins toward centers of surface activated platelets. Instead, they entered channels of the surface-connected open canalicular system (OeS) in over 40% of dendritic platelets and 5% to 15% of fully spread platelets [27,32,36]. Instead, they entered channels of the surface-connected open canalicular system (OeS) in over 40% of dendritic platelets and 5% to 15% of fully spread platelets [27,32,36].…”