Phosphatidylcholine metabolism in human endothelial cells: Modulation by phosphocholine

Phosphatidylcholine is the principal phospholipid in mammalian tissues, and a major source for the production of arachidonic acid. In this study, the effect of exogenous phosphocholine, a precursor of phosphatidylcholine bios ynthesis, on the metabolism of phosphatidylcholine in human umbilical vein endothelial cells was investigated. Incubation of endothelial cells with ex ogenous phosphocholine at concentrations of 1 to 5 mM was found to inhibit choline uptake and its subsequent incorporation into phosphatidylcholine. P hosphocholine appeared to inhibit choline uptake in a competitive manner. S ince phosphatidylcholine is metabolized mainly by the action of phospholipa se A(2), with the release of arachidonic acid and other fatty acids, the ef fect of phosphocholine on arachidonic acid release in endothelial cells was also examined. The induction of arachidonic acid release by ATP was enhanc ed in cells treated with 1 mM phosphocholine. In vitro assays of phospholip ase A(2) activity in cells incubated with phosphocholine, however, did not produced any significant change in the activity of this enzyme. The results of this study show that phosphocholine modulates the biosynthesis and cata bolism of phosphatidylcholine in an indirect manner.