Tertov VV, Orekhov AN
Chem Phys Lipids 1994 Jan 67-68: 161-6
The effect of Lp(a) on lipid metabolism in cells cultured from unaffected human aortic intima has been investigated. Lp(a) isolated from the blood of healthy subjects failed to alter intracellular neutral lipid content. On the other hand, Lp(a) obtained from coronary atherosclerosis patients induced a 1.5- to 2-5-fold increase in intracellular levels of free and esterified cholesterol and triglycerides. The sialic acid content of patients' Lp(a) was 2.5-fold lower as compared with that of healthy subjects' Lp(a). Healthy donors' Lp(a) in vitro desialylated with neuraminidase were able to accumulate lipids within the cells. Using lectin-chromatography on Ricinus Communis agglutinin-agarose, Lp(a) was divided into subfractions differing by sialic acid content. Desialylated (sialic acid-poor) Lp(a), but not sialylated lipoproteins, were capable of increasing the intracellular content of total cholesterol. Desialylated but not sialylated Lp(a) formed aggregates during incubation under cell culture conditions. Isolated aggregates of desialylated Lp(a) induced lipid accumulation in cells. Elimination of Lp(a) aggregates from cultural medium prevented the increase of intracellular lipids. Complexes of Lp(a) with the matrix components and antibodies increased lipid level in cultured cells. We assume that formation of large particles of desialylated Lp(a) aggregates or Lp(a)-containing complexes is a necessary step for lipid accumulation in human intimal cells.