Propionic acid‐induced calcium mobilization in human neutrophils
- 1 July 1988
- journal article
- research article
- Published by Wiley in Journal of Cellular Physiology
- Vol. 136 (1) , 118-124
- https://doi.org/10.1002/jcp.1041360115
Abstract
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.This publication has 38 references indexed in Scilit:
- Phosphorylation of ras oncogene product by protein kinase CBiochemical and Biophysical Research Communications, 1987
- The kinetics of calcium binding to fura‐2 and indo‐1FEBS Letters, 1987
- Two roles for guanine nucleotides in the stimulus-secretion sequence of neutrophilsNature, 1986
- Measurement of ionized calcium in blood platelets with a new generation calcium indicatorBiochemical and Biophysical Research Communications, 1985
- Pertussis but not cholera toxin inhibits the stimulated increase in actin association with the cytoskeleton in rabbit neutrophils: Role of the “G proteins” in stimulus-response couplingBiochemical and Biophysical Research Communications, 1985
- Protein kinase C as a bidirectional regulator of cell functionTrends in Pharmacological Sciences, 1985
- Pertussis toxin inhibits the rise in the intracellular concentration of free calcium that is induced by chemotactic factors in rabbit neutrophils: Possible role of the “G proteins” in calcium mobilizationBiochemical and Biophysical Research Communications, 1984
- Amiloride-sensitive Na+/H+ exchange in human neutrophils: Mechanism of activation by chemotactic factorsBiochemical and Biophysical Research Communications, 1984
- Direct demonstration of increased intracellular concentration of free calcium in rabbit and human neutrophils following stimulation by chemotactic factorBiochemical and Biophysical Research Communications, 1983
- Specific modulation of the intracellular pH of rabbit neutrophils by chemotactic factorsBiochemical and Biophysical Research Communications, 1980