Breakdown of a phosphatidylcholine pool arising from the metabolic conversion of phosphatidylethanolamine as a novel source of diacylglycerol in activated T cells.

Abstract

Activation of Jurkat T cells with either phytohemagglutinin (PHA), CD3 or CD2 monoclonal antibodies (mAbs) induces the production of diacylglycerol (DAG) from two different sources. Activation of the phosphatidylinositide cycle in activated T cells is a well-known source of the second messengers DAG and inositol triphosphate (IP3). The present report demonstrates that a particular pool of phosphatidylcholine (PC) arising from the sequential methylation of phosphatidyl-ethanolamine (PE) is probably a second source of DAG. The occurrence of two distinct sources of DAG in activated T cells is supported by the fact that DAG production was not accompanied by a decrease of phosphatidylinositol mono- and bisphosphate (PIP/PIP2) pools as measured after [3H]glycerol labeling whereas [3H]arachidonic acid PIP/PIP2 pools decrease in parallel with DAG production. The presence of a second generating pathway for DAG was demonstrated by measuring phospholipid synthesis and degradation in cells labeled with [3H]choline, [3H]ethanolamine or [3H]serine. In Jurkat cells, PHA decreased the incorporation of [3H]ethanolamine and [3H]serine but not [3H]choline into PC suggesting that the PC pool arising from the methylation of PE was utilized during activation whereas the PC pool synthesized through the CDP choline pathway was not. In [3H]ethanolamine-prelabeled cells, but not in [3H]choline-prelabeled cells, PHA, CD3 and CD2 induced the breakdown of PC. The PC breakdown was accompanied by a release of [3H]choline and the production of DAG and phosphatidic acid (PA). The breakdown of PC described in the present report strongly suggests that PC participates in T lymphocyte activation through the production of DAG.