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Contribution of HDL‐apolipoproteins to the inhibition of low density lipoprotein oxidation and lipid accumulation in macrophages
Author(s) -
Lin KaeYuan,
Chen YuhLien,
Shih ChunChe,
Pan JuPin,
Chan WoanEng,
Chiang AnNa
Publication year - 2002
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.10210
Subject(s) - foam cell , tbars , chemistry , cholesterol , apolipoprotein b , lipoprotein , macrophage , in vitro , biochemistry , high density lipoprotein , oxidative phosphorylation , medicine , low density lipoprotein , endocrinology , lipid peroxidation , oxidative stress , biology
High‐density lipoprotein (HDL) is known as a protective factor against atherosclerosis. However, whether HDL‐apolipoproteins (apo‐HDL) contribute to the protection in arterial cells remains unclear. The localization patterns of human apolipoproteins in atherosclerotic arteries were determined using immunohistochemical examination. The results indicate that several apolipoproteins are retained in component cells of the coronary artery walls. To elucidate the possible roles of apo‐HDL in the protection of atherosclerotic lesion formation, we investigated the effects of apo‐HDL on the formation of conjugated diene (CD) in a cell‐free system and thiobarbituric acid‐reactive substances (TBARS) in the medium of a macrophage‐mediated LDL oxidation system. The results showed that apo‐HDL significantly exerted an inhibitory effect on LDL lipid oxidation in vitro. In addition, apo‐HDL decreased cholesterol influx but enhanced cholesterol efflux from J774 macrophages in a dose‐dependent manner. These results are consistent with the notion that there is reduced intracellular lipid accumulation in apo‐HDL treated macrophages. These data provide a direct evidence for apo‐HDL in protecting LDL from oxidative modification and in reducing the accumulation of cholesterol and lipid droplets by J774 macrophages. J. Cell. Biochem. 86: 258–267, 2002. © 2002 Wiley‐Liss, Inc.