Rotheneder M, Krempler F, Kostner G M
Institute of Medical Biochemistry, University of Graz, Austria.
Ann Biol Clin (Paris). 1988;46(1):30-4.
In this study we tried to elucidate the atherogenicity of various plasma lipoproteins with respect to their capability of foam cell formation. Mouse peritoneal macrophages (MPM) were incubated with increasing amounts of lipoproteins and the incorporation of 14C oleate into the cholesteryl ester fraction was followed. The results may be summarized as follows: freshly isolated Lp(a) behaves very similar to normal LDL causing no or little increase in CE formation in MPM. Lp(a) treated with dextran sulfate as well as with antibodies to Apo-a, strongly interact with scavenger receptors causing massive accumulation of CE in MPM. The abnormal lipoproteins from patients suffering from liver disease, LP-X, HDL-E cause no increase in CE formation of MPM. They behave very similar to artificial PL/FC liposomes. If on the other hand these abnormal lipoproteins are mixed with Ac-LDL, a synergistic effect was observed causing an approx. 30 per cent increase in CE-formation as compared to Ac-LDL alone. This was caused by a net transfer of FC from abnormal lipoproteins to Ac-LDL alone. This was caused by a net transfer of FC from abnormal lipoproteins to Ac-LDL. It is concluded that the lipoproteins studied in this report by itself exert no atherogenic function in MPM. They may, however, aggravate the atherogenicity of other processes known to be involved in the development of vascular diseases.
