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Phosphatidic acid induces calcium influx in neutrophils via verapamil‐sensitive calcium channels
Author(s) -
Siddiqui Rafat A.,
Burtschi Daniel J.,
Kovacs Richard
Publication year - 2000
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(20000801)78:2<297::aid-jcb11>3.0.co;2-7
Subject(s) - verapamil , phosphatidic acid , extracellular , intracellular , chemistry , phospholipase d , channel blocker , calcium , phospholipase , depolarization , calcium in biology , stimulation , phospholipase c , voltage dependent calcium channel , endogeny , biophysics , microbiology and biotechnology , biochemistry , endocrinology , biology , signal transduction , membrane , enzyme , phospholipid , organic chemistry
Phosphatidic acid (PA) induces a biphasic Ca 2+ mobilization response in human neutrophils. The initial increase is due to the mobilization of Ca 2+ from intracellular stores, whereas the secondary increase is due to the influx of Ca 2+ from extracellular sources. The present investigation characterizes PA‐induced Ca 2+ influx in neutrophils. Depolarization of neutrophils by 50 mM KCl enhanced PA‐induced Ca 2+ influx, whereas verapamil, a Ca 2+ channel blocker, attenuated this response in a dose‐dependent manner. These observations suggest that PA‐induced Ca 2+ influx is mediated via verapamil‐sensitive Ca 2+ channels. Stimulation of neutrophils with exogenous PA results in accumulation of endogenously generated PA with a time course similar to the effects of exogenous PA on Ca 2+ influx. Ethanol inhibited the accumulation of endogenous PA and calcium mobilization, indicating that activation of membrane phospholipase D plays a role in PA‐mediated Ca 2+ influx. The results of this study suggest that exogenously added PA stimulates the generation of intracellular PA, which then mediates Ca 2+ influx through verapamil‐sensitive Ca 2+ channels. J. Cell. Biochem. 78:297–304, 2000. © 2000 Wiley‐Liss, Inc.