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Metabolic inhibitors as tools to delineate participation of distinct intracellular pathways in enhancement of lactose‐induced dissociation of neutrophil and thymocyte aggregates formed by mediation of a plant lectin
Author(s) -
Timoshenko A. V.,
Gorudko I. V.,
Kaltner H.,
Cherenkevich S. N.,
Gabius H. J.
Publication year - 1997
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549700204271
Subject(s) - lectin , intracellular , thymocyte , chemistry , biochemistry , concanavalin a , microbiology and biotechnology , cell , c type lectin , nordihydroguaiaretic acid , biophysics , enzyme , biology , t cell , immune system , lipoxygenase , in vitro , immunology
Signaling processes in the course of the formation of the lectin‐mediated aggregates may partake in conveying enhanced stability to the cell clusters. To prove the validity of this reasoning in a model, we have studied the impact of addition of three metabolic inhibitors (N‐ethylmaleimide, nordihydroguaiaretic acid, and trifluoperazine on lactose‐dependent dissociation of cell aggregates, formed in the presence of the galactoside‐binding mistletoe lectin. Using both human neutrophils and rat thymocytes to avoid measurement of responses restricted to a single cell type, an enhanced dissociation of lectin‐formed cell aggregates was observed, when lactose and an inhibitor were present. Among the tested inhibitors, nordihydroguaiaretic acid and N‐ethylmateimide were more potent enhancers of cell dissociation than trifluoperazine. These results suggest that biosignaling pathways connected with lipoxygenase activity as well as the level of intracellular sulfhydryl groups confer further stability to lectin‐dependent cell aggregates. The systematic evaluation of inhibitors for defined activities is thus suggested as a tool to disclose the nature and the contribution of individual signaling mechanisms to post‐binding effects following lectin‐initiated cell contact formation.