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The phosphatidylcholine pathway of diacylglycerol formation stimulated by phorbol diesters occurs via phospholipase D activation
Author(s) -
Cabot Myles C.,
Welsh Clement J.,
Cao Hui-ting,
Chabbott Holly
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)81374-7
Subject(s) - diacylglycerol kinase , phosphatidate , phosphatidylcholine , phospholipase c , phosphocholine , biochemistry , diglyceride , myristic acid , phospholipase d , protein kinase c , chemistry , choline , phosphatidylethanol , phospholipase , phospholipase a2 , enzyme , phospholipid , fatty acid , palmitic acid , membrane
Agonist‐induced degradation of phosphatidylcholine (PC) is of interest as this pathway of diacylglycerol (DG) generation may provide added opportunities for the regulation of protein kinase C (PKC). In REF52 cells [ 3 H]myristic acid is preferentially incorporated into PC; this, coupled with the use of [ 3 H]choline, allows for quantitation of both the water‐soluble and the lipid products generated when PC is degraded. In cells prelabeled with [ 3 H]choline, TPA stimulated a time‐dependent release, into the medium, of choline and not phosphocholine or glycerophosphocholine. Treatment of [ 3 H]myristic acid‐labeled cells with either phorbol diesters, sn ‐1,2‐dioctanoylglycerol, or vasopressin elicited the formation of labeled phosphatidate (PA) and DG. The temporal pattern of PC hydrolysis in cells treated with TPA is indicative of a precursor (PA)‐product (DG) relationship for an enzymatic sequence initiated by phospholipase D. Adding propranolol, a phosphatidate phosphohydrolase inhibitor, eliminated TPA‐induced DG formation, whereas PA generation was unaffected. From these data we conclude that TPA elicits DG formation from PC by the sequential actions of phospholipase D and phosphatidate phosphohydrolase.