The role of galectin-3 in endocytosis of advanced glycation end products and modified low density lipoproteins

被引：95

作者：

Zhu, WQ ^{[1
]}

Sano, H ^{[1
]}

Nagai, R ^{[1
]}

Fukuhara, K ^{[1
]}

Miyazaki, A ^{[1
]}

Horiuchi, S ^{[1
]}

机构：

[1] Kumamoto Univ, Sch Med, Dept Biochem, Kumamoto 8600811, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 280卷 / 04期

关键词：

galectin-3; AGE; AGE-receptors; scavenger receptor class A (SR-A); modified LDLs; foam cells; atherosclerosis;

D O I：

10.1006/bbrc.2001.4256

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Galectin-3, a member of beta -galactoside-binding lectin family, is suggested to be an AGE-receptor. To examine this possibility, we prepared CHO cells overexpressing human galectin-3 (galectin-3-CHO cells). Galectin-3-CHO cells showed a specific and saturable binding to I-125-AGE-BSA with Kd of 3.1 mug/ml. I-125-AGE-BSA was endocytosed by galectin-3-CHO cells and underwent lysosomal degradation. The endocytosis of I-125-AGE-BSA was inhibited not only by unlabeled AGE-BSA but also by acetylated LDL and oxidized LDL, ligands for the scavenger receptor family. Furthermore, I-125-oxidized LDL and I-125-acetylated LDE were actively endocytosed by galectin-3-CHO cells and the incubation with acetyl-LDL led to intracellular accumulation of cholesteryl esters, indicating the role of galectin-3 in endocytosis of AGE-proteins and modified LDLs. Since galectin-3 was localized and upregulated in foam cells at human atherosclerotic lesions, the present results suggest that galectin-3 plays an important role in formation of atherosclerotic lesions in vivo, by modulating endocytic uptake of AGE-proteins and modified LDLs. (C) 2001 Academic Press.

引用

页码：1183 / 1188

页数：6

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