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Phosphatidic acid induces calcium influx in neutrophils via verapamil-sensitive calcium channels
Authors:Siddiqui R A  Burtschi D J  Kovacs R
Institution:Cellular Biochemistry Laboratory, Methodist Research Institute, Indianapolis, Indiana. rsiddiqu@clarian.com
Abstract: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.
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