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Wheat Germ Agglutinin-Induced Intracellular Calcium Mobilization in Human Platelets: Suppression by Staurosporine and Resistance to Cyclic AMP Inhibition

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Abstract

The lectin wheat germ agglutinin (WGA) elicited a prompt and sharp increase in intracellular Ca2+ concentration in human platelets. The WGA- induced Ca2+ mobilization was markedly inhibited by a protein kinase inhibitor staurosporine, whereas Ca2+ mobilization by receptor-mediated agonists, including thrombin, platelet-activating factor, and arginine-vasopressin, was not. In contrast, the lectin-induced Ca2+ mobilization was resistant to cyclic AMP inhibition, compared with that induced by receptor-mediated agonists. These findings indicate that the mechanism of intracellular Ca2+ mobilization, or possibly phospholipase C activation, induced by WGA is different from that induced by receptor-mediated agonists in human platelets.

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Cited by (17)

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    Gong et al. have shown that Con A binds to LFA-1, that leads to the internalization of Con A and activates NLRP3 inflammasome through endoplasmic reticulum stress and subsequently leads to the release of proinflammatory cytokines like IL-1β and IL-18 (Gong et al., 2017). Con A and WGA are also reported to induce intracellular Ca2+ mobilization in different cell types that is hypothesized to be a mechanism of NLRP3 inflammasome activation (Grinstein et al., 1987; Yatomi et al., 1993). Dioclea violacea (Dvl), a lectin isolated from the Fabaceae family is reported to have anti-inflammatory properties whereby it inhibits neutrophil migration upon inflammation when injected intravenously (Nascimento et al., 2018; Freitas et al., 2015).

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    VAA has not been so far used to study changes of blood cells from patients with ACS, whereas the application of WGA and some other plant lectins as aggregants was reported recently (11). VAA and WGA, however, are not only able to induce cell aggregation but can also serve as potent stimuli of various signaling responses in cells including intracellular Ca2+ mobilization (29,30), generation of reactive oxygen species (30), upregulation of tyrosine and other protein kinases (31,32) as well as cytoskeleton perturbations (33,34). Most important is that all these lectin-induced changes may result in activation/expression of additional adhesion proteins on the cell surface allowing for stabilization of intracellular contacts and cell aggregates (12-17).

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