Isolation of lipoprotein-proteoglycan complexes from balloon catheter deendothelialized aortas and the uptake of these complexes by blood monocyte-derived macrophages.

Lipoprotein-Proteoglycan (LP-PG) complexes from the neointima, developed in response to injury, were studied to examine their ability to stimulate lipid accumulation in blood monocyte-derived macrophages (BMDM). LP-PG complexes were extracted from intimal-medial tissues from normal and balloon catheter deendothelialized aortas of normocholesterolemic rabbits, in 0.16 M NaCl for 24 h at 4 degrees C. The extract was purified through an anti-apo-B affinity column. Adsorbed material dissociated with 4 M Gu-HCI buffer was analyzed for lipoproteins (LP) and glycosaminoglycans (GAG). Results demonstrated that LP-PG complexes consisted of apo-B associated with chondroitin sulfate and hyaluronic acid. BMDM were incubated with 125I-LP, 125I-LP-NPG (from normal aortas) or 125I-LP-IPG (from injured aortas) for 20 h at 37 degrees C. LP binding, internalization and degradation was markedly increased for LP-NPG and LP-IPG over native LP. Phagocytosis appeared to be the primary route of uptake of LP-PG complexes. Competition experiments indicated that about 40% of the uptake of LP-PG complexes is mediated by the apo-B/E receptor pathway. The scavenger receptor played a minor part in the uptake of LP-PG complexes. Data from this study indicate that LP-PG complexes are present in normal and injured aortas of normocholesterolemic rabbits and these complexes accelerate LP uptake by BMDM more than native LP. Therefore, LP-PG complexes may contribute to lipid accumulation by BMDM, thus generating foam cells. Furthermore, LP-PG complexes prepared from PG of injured aortas are more effective in lipid accumulation than LP-PG complexes from PG of normal aortas.