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.