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Propionic acid‐induced calcium mobilization in human neutrophils
Author(s) -
Naccache Paul H.,
Faucher Nicole,
Caon Adriana C.,
McColl Shaun R.
Publication year - 1988
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041360115
Subject(s) - calcium , pertussis toxin , leukotriene b4 , chemistry , phorbol , protein kinase c , biochemistry , platelet activating factor , cholera toxin , endocrinology , biology , receptor , g protein , kinase , inflammation , immunology , organic chemistry
The ability of propionic acid to elicit an increase in the level of cytoplasmic free calcium in human neutrophils was examined in detail. Propionic acid induced a rapid and dose‐dependent mobilization of calcium that relied on both internal and external sources of calcium. The effects of propionic acid on the mobilization of calcium were inhibited by pertussis toxin, but not cholera toxin, implicating a guanine nucleotide binding protein. Furthermore, preincubation of the neutrophils with phorbol 12‐myristate 13‐acetate resulted in a decreased mobilization of calcium. This inhibitory activity of phorbol myristate acetate was antagonized by the protein kinase C inhibitor H‐7. Preincubation of the cells with the synthetic chemotactic factor fMet‐Leu‐Phe caused a reduction in the magnitude of the calcium transient elicited by propionic acid. However, the calcium response to propionic acid was not affected by antagonists of fMet‐Leu‐Phe and platelet‐activating factor binding or by an inhibitor of leukotriene synthesis. Propionic acid did not elicit a mobilization of calcium in monocytes, platelets, lymphocytes, or undifferentiated HL‐60 cells. However, the treatment of the HL‐60 cells with dimethylsulfoxide resulted in the appearance of a calcium response to propionic acid. The potential physiological significance of these findings are discussed.