IgE-mediated histamine release in rat basophilic leukemia cells: receptor activation, phospholipid methylation, Ca2+ flux, and release of arachidonic acid |
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| Authors: | F T Crews Y Morita A McGivney F Hirata R P Siraganian J Axelrod |
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| Institution: | 1. Section on Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health, U.S.A.;1. Clinical Immunology Section, Laboratory of Microbiology and Immunology, National Institute of Dental Research, Bethesda, Maryland 20205 U.S.A. |
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| Abstract: | Stimulation of IgE receptors on rat basophilic leukemia cells causes a transient rise and fall of methylated phopholipids, Ca2+ influx, and release of arachidonic acid previously incorporated into phosphatidylcholine and liberation of histamine. Inhibition of phospholipid methylation by methyltransferase inhibitors, 3-deazaadenosine and homocysteine thiolactone, almost completely blocks the influx of Ca2+, and release of arachidonic acid and histamine. Stimulation of immunoglobulin E receptors by antigen releases only 14C]arachidonic acid but not 14C]linoleic acid, 14C]oleic acid and 14C]stearic acid, all of which were previously incorporated into phospholipids. 14C]Arachidonate was found to be incorporated mainly into phosphatidylcholine. The phosphatidycholine rich in arachidonate appeared to be synthesized to a considerable extent by the transmethylation pathway. These findings suggest that in rat basophilic leukemia cells, immunoglobulin E receptors, phospholipid methyltransferases, Ca2+ ion channel, and phospholipase(s) that cause release of arachidonic acid and the discharge of histamine are associated. |
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