title: Metabolism of human plasma triacylglycerol-rich lipoproteins in rodent macrophages: capacity for interaction at beta-VLDL receptor.
abstract: The capacity of human plasma triacylglycerol-rich lipoproteins to be metabolized by rat macrophages was studied with plasma triacylglycerol-rich lipoproteins obtained from subjects with fasting chylomicronemia or from normal subjects after a fat meal. Triacylglycerol-rich lipoproteins were separated by chromatography into two fractions designated TRL1 and TRL2; from their composition and changing concentration during alimentary lipemia, TRL1 contained a higher proportion of chylomicron remnants than TRL2. Degradation of 125I-labeled TRL1 was greater than that of 125I-labeled TRL2. In competition studies with 125I-labeled beta-VLDL from cholesterol-fed rabbits, unlabeled TRL1 displaced beta-VLDL as completely as did unlabeled beta-VLDL, being slightly more potent than TRL2, which contained less apolipoprotein E than TRL1. This reflected common interaction at receptors that probably included both beta-VLDL and B/E receptors, since: (1) in fresh macrophages, VLDL from hypertriglyceridemic subjects partially displaced beta-VLDL; (2) in B/E receptor-repressed macrophages, TRL1 maintained capacity to totally displace beta-VLDL. This was confirmed in experiments with J774 murine macrophages in which triacylglycerol-rich lipoproteins and beta-VLDL displaced each other equally, whereas LDL was ineffective in displacing beta-VLDL. Furthermore, monoclonal antibodies raised against apolipoprotein B48 and reacting strongly with LDL, failed to inhibit the binding of triacylglycerol-rich lipoprotein to the macrophages. This indicates an interaction through apolipoprotein E which is present in high concentration in triacylglycerol-rich lipoprotein as well as in beta-VLDL. It applies to triacylglycerol-rich particles derived from either the intestine (chylomicron remnants) or the liver (VLDL remnants from hypertriglyceridemic subjects).
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000276:immunology; D001056:Apolipoproteins C / Q000302:isolation & purification; D001057:Apolipoproteins E / Q000378:metabolism; D002784:Cholesterol / Q000032:analysis; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism; D008074:Lipoproteins / Q000378:metabolism*; D053419:Lipoproteins, IDL; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011817:Rabbits; D051381:Rats; D011973:Receptors, LDL / Q000378:metabolism*; D014280:Triglycerides / Q000032:analysis
chemical_list: D000911:Antibodies, Monoclonal; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D001056:Apolipoproteins C; D001057:Apolipoproteins E; D008074:Lipoproteins; D053419:Lipoproteins, IDL; D011973:Receptors, LDL; D014280:Triglycerides; C036053:VLDL receptor; D002784:Cholesterol