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Phosphatidylinositol turnover in human monocyte‐derived macrophages by native and acetyl LDL
Author(s) -
Ishikawa Yuichi,
Asaoka Yoshinori,
Taniguchi Takahiro,
Tsunemitsu Masahiko,
Fukuzaki Hisashi
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80248-0
Subject(s) - phosphatidylinositol , chemistry , scavenger receptor , incubation , monocyte , macrophage , receptor , biochemistry , inositol , hydrolysis , in vitro , cholesterol , medicine , signal transduction , lipoprotein
Monocyte‐derived macrophages play a key role in pathogenesis of atherosclerosis. However, the mechanism of activating macrophages in atheromatous lesions has not been fully investigated. This report describes the contribution of phosphatidylinositol turnover to the uptake of low density lipoproteins (LDL) by macrophages. Both native and acetyl LDL stimulated inositol 1,4,5‐triphosphate (IP 3 ) formation in a dose‐dependent manner at concentrations of 0–70 μg/ml. The potency of IP 3 formation by acetyl LDL (0.44 nmol/mg protein) was 2‐fold higher than that by native LDL (0.21 nmol/mg protein). Time course studies showed that a maximal effect of IP 3 formation by acetyl LDL at concentrations of 30 μg/ml was observed at 3 min. Longer incubation diminished IP 3 formation. Oxidized LDL also stimulated IP 3 formation with a similar efficiency to acetyl LDL. It was indicated that chemically modified LDL which were taken up through the scavenger receptor pathway activated the macrophages by mediating the phosphatidylinositol hydrolysis and IP 3 formation.