Role of the macrophage galactose lectin in the uptake of desialylated LDL

Citation
Al. Bartlett et al., Role of the macrophage galactose lectin in the uptake of desialylated LDL, ATHEROSCLER, 153(1), 2000, pp. 219-230
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
ATHEROSCLEROSIS
ISSN journal
00219150 → ACNP
Volume
153
Issue
1
Year of publication
2000
Pages
219 - 230
Database
ISI
SICI code
0021-9150(200011)153:1<219:ROTMGL>2.0.ZU;2-M
Abstract
Desialylated low density lipoprotein (LDL) is rapidly taken up and accumula ted by both peripheral blood monocytes and cells isolated from human arteri al intima consisting predominantly of smooth muscle cells. It is shown that thioglycollate (TG)-elicited mouse macrophages and mouse peritoneal macrop hages stimulated with lipopolysaccharide (LPS) show increased expression of a membrane-bound, galactose-specific lectin that could be responsible for this uptake. In LPS-stimulated macrophages accumulation of desialylated LDL is increased ca. 2.6-fold. Accumulation of acetylated LDL in the same cell s is reduced, suggesting that the galactose-specific lectin might be respon sible for the uptake of desialylated LDL. Transfection of cells with the mo use macrophage Gal/GalNAc-specific lectin (MMGL) increased their capacity t o take up asialofetuin (ASF) and, to a smaller extent, desialylated LDL. Th e uptake of desialylated LDL was small, most likely due to the high k(d) of MMGL for biantennary oligosaccharides as found on LDL, and low concentrati on of LDL achieved in tissue culture experiments. The data suggest that the expression of galactose-specific lectins can be elevated under inflammator y conditions, and that these receptors could contribute to foam cell format ion under conditions of high desialylated LDL concentration, as might be fo und in arterial intima. (C) 2000 Elsevier Science ireland Ltd. All rights r eserved.