title: Stimulation of phospholipid methylation, Ca2+ influx, and histamine release by bridging of IgE receptors on rat mast cells.
abstract: Normal rat mast cells were stimulated by antibodies against IgE receptors (anti-RBL) or by anti-IgE, and [3H]methyl group incorporation into phospholipids, 45Ca uptake, and histamine release were examined. Anti-RBL or its F(ab')2 fragments and anti-IgE induced an increase in the incorporation of [3H]methyl into phospholipids, in 45Ca influx, and in histamine release. By contrast, Fab' monomer fragments of anti-RBL induced none of these reactions. The transient increase of [3H]methyl incorporation in lipids peaked within 15 sec after the addition of either anti-RBL or anti-IgE and fell to basal level in 30 sec. This was then followed by an influx of 45Ca that increased to a maximum in 2 min and by histamine release that reached a maximum in 3 min. Inhibition of phospholipid methylation resulted in an inhibition of 45Ca influx and histamine release. These findings demonstrate that phospholipid methylation in rat mast cells is induced by bridging of IgE receptors on the cell surface and that increased methylation of phospholipids sets the stage for an influx of Ca2+ and subsequent release of histamine.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D006636:Histamine Release; D007073:Immunoglobulin E; D007140:Immunoglobulin Fab Fragments; D008407:Mast Cells / Q000378:metabolism*; D008563:Membrane Lipids / Q000378:metabolism; D008745:Methylation; D008780:Methyltransferases / Q000037:antagonists & inhibitors; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D011971:Receptors, Immunologic / Q000502:physiology*; D014372:Tubercidin / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D007140:Immunoglobulin Fab Fragments; D008563:Membrane Lipids; D010743:Phospholipids; D011971:Receptors, Immunologic; D007073:Immunoglobulin E; C017194:5'-deoxy-5'-(isobutylthio)-3-deazaadenosine; D008780:Methyltransferases; D014372:Tubercidin; D002118:Calcium