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Enhanced macrophage uptake of lipoprotein(a) after Ca 2+ ‐induced aggregate‐formation
Author(s) -
Tanaka Seiya,
Yashiro Akira,
Tasaki Hiromi,
Nakashima Yasuhide
Publication year - 1998
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-998-0219-5
Subject(s) - chemistry , lipoprotein , phagocytosis , cholesterol , lipoprotein(a) , cytochalasin d , macrophage , cytochalasin b , foam cell , lipidology , biochemistry , chromatography , immunology , cell , in vitro , biology , cytoskeleton
We tested the hypothesis that aggregated lipoprotein(a) [Lp(a)] is avidly taken up by macrophages. Lp(a) was isolated by sequential centrifugations and gel chromatography from a patient with high plasma levels of Lp(a) who was being treated with low density lipoprotein (LDL)‐apheresis. Aggregated Lp(a) was prepared by mixing native Lp(a) with 2.5 mmol/L CaCl 2 , and 54% of the 125 I‐Lp(a) aggregated after interacting with CaCl 2 . The binding and degradation of aggregated Lp(a) in macrophages were 4.6‐ and 4.7‐fold higher than those of native Lp(a), respectively. An excess amount of LDL did not inhibit either increase. Cholesterol esterification in macrophages was markedly stimulated by aggregated Lp(a), and macrophages were transformed into foam cells. Cytochalasin B, a phagocytosis inhibitor, strongly inhibited the degradation and cholesterol esterification (78 and 83%, respectively). These findings suggested that aggregation may be partially involved in Lp(a) accumulation, thereby contributing to the acceleration of atherosclerosis.