Phosphatidylinositol turnover in mitogen-activated lymphocytes. Suppression by low-density lipoproteins

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Abstract
Low-density lipoproteins [LDL] inhibit phytohemagglutinin-enhanced turnover of phosphatidylinositol [PI] in human peripheral lymphocytes. Turnover was assessed by 32P incorporation into phospholipids and by a loss of 32P from [32P]PI. Inhibition of lipid turnover by LDL is not the result of a change in the amount of phytohemagglutinin required for maximum cellular response. Neither phytohemagglutinin nor LDL influence 32P incorporation into phosphatidylethanolamine and phosphatidylcholine during the 1st 60 min after mitogenic challenge. The extent of inhibition of PI turnover by LDL depends on the concentration of LDL present in the incubation medium; 50% of maximum inhibition occurs at a LDL protein concentration of 33 .mu.g/ml and maximum inhibition occurs at LDL protein concentrations above 100 .mu.g/ml. Phytohemagglutinin stimulates 32P incorporation into PI, PI phosphate and PI bisphosphate. However, LDL abolish 32P incorporation into PI without affecting incorporation into PI phosphate and PI bisphosphate. The ability of LDL to inhibit phytohemagglutinin-induced PI turnover is mimicked by EGTA [ethylene glycol bis[2-aminoethyl ether]-N,N''-tetraacetic acid]. Inhibition of LDL by phytohemagglutinin-induced 32P incorporation into PI correlated directly with inhibition by LDL of Ca2+ accumulation. Ca2+ accumulation and turnover of PI may be coupled responses in lymphocytes challenged by mitogens. The step in PI metabolism that is sensitive to LDL and that is coupled to Ca2+ accumulation is release of [32P]PI from PI.

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