Premium
Transient inhibition of capacitative calcium entry in human neutrophils by a monoclonal antibody directed against a 19‐kDa antigen
Author(s) -
Alonso Maria Teresa,
Mollinedo Faustino,
Barasoain Isabel,
Alvarez Javier,
GarciaSancho Javier
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.60.3.323
Subject(s) - pertussis toxin , biology , thapsigargin , n formylmethionine leucyl phenylalanine , cholera toxin , intracellular , tyrosine phosphorylation , phospholipase c , chemotaxis , microbiology and biotechnology , monoclonal antibody , tyrosine kinase , g protein , phosphorylation , biochemistry , signal transduction , antibody , endocrinology , receptor , immunology
P1C3 is a monoclonal antibody that binds p19, a novel neutrophil activation antigen that translocates to the cell surface upon neutrophil activation. We find that P1C3 inhibits capacitative Ca 2+ entry, induced by emptying the intracellular Ca 2+ stores with thapsigargin. The effect is transient, reaching its maximum at 30–60 s, but becomes permanent upon pretreatment of the cells with the protein phosphatase inhibitor calyculin A, suggesting the involvement of protein phosphorylation. The inhibitory action is similar to the one reported previously for the chemotactic peptide N ‐formyl‐methionyl‐leucyl‐phenylalanine (fMLP), although the transduction mechanism may be different. Inhibition of Ca 2+ entry by fMLP was prevented by pretreatment with pertussis toxin, whereas inhibition by P1C3 was not. Pretreatment with cholera toxin had no effect. This suggests that the effect of P1C3 may not be mediated by a heterotrimeric G protein. Tyrosine kinase inhibitors did not prevent inhibition by either fMLP or P1C3. Phospholipase C activation seems not to be involved as P1C3, contrarily to fMLP, was unable to induce Ca 2+ release from the intracellular Ca 2+ stores. J. Leukoc. Biol . 60: 323–327; 1996.