Endocytic uptake of advanced glycation endproducts by mouse liver sinusoidal endothelial cells is mediated by a receptor distinct from the class A scavenger receptor

• Published in: International Congress series 2002-11, Vol.1245, p.157-162
• Main Authors: Matsumoto, Kenshi, Nagai, Ryoji, Masunaga, Kouichi, Yoshida, Masaki, Ueda, Shoichi, Smedsrød, Bård, Horiuchi, Seikoh
• Format: Article
• Language: English
• Subjects: Advanced glycation endoproducts; Endocytosis; Formaldehyde-treated albumin; Liver sinusoidal endothelial cell; Macrophage scavenger receptor class A
• ISSN: 0531-5131; 1873-6157
• DOI: 10.1016/S0531-5131(02)00907-X

Previous studies using peritoneal macrophages obtained from macrophage scavenger receptor-A (MSR-A)-knockout mice showed that the endocytic uptake of advanced glycation endproducts (AGE) by macrophages was mainly mediated by MSR-A. However, it is controversial whether the endocytic uptake of intravenously injected AGE-proteins by liver endothelial cells (LECs) is similarly explained by receptor-mediated endocytosis via MSR-A. The present study was conducted to compare the capacity to endocytose AGE-proteins in LECs and peritoneal macrophages obtained from MSR-A-knockout and litter mate wild type mice. The endocytic degradation of MSR-A-knockout LECs for AGE-BSA was indistinguishable from that of wild type LECs, whereas that of MSR-A-knockout peritoneal macrophages for AGE-BSA was reduced to 30% of wild type cells. Furthermore, formaldehyde-treated serum albumin (f-Alb), a ligand known to undergo scavenger receptor-mediated endocytosis by LECs, was effectively taken up by MSR-A-knockout LECs at a capacity that did not differ from that of wild type LECs. Furthermore, the endocytic uptake of AGE-BSA by LECs was effectively competed for by unlabelled f-Alb. These data indicate that the scavenger receptor-ligands AGE-proteins are endocytosed by LECs through a non-MSR-A pathway.