Insulin enhances macrophage scavenger receptor-mediated endocytic uptake of advanced glycation end products.

The Journal of Biological Chemistry
H SanoS Horiuchi

Abstract

Hyperglycemia accelerates the formation and accumulation of advanced glycation end products (AGE) in plasma and tissue, which may cause diabetic vascular complications. We recently reported that scavenger receptors expressed by liver endothelial cells (LECs) dominantly mediate the endocytic uptake of AGE proteins from plasma, suggesting its potential role as an eliminating system for AGE proteins in vivo (Smedsrod, B., Melkko, J., Araki, N., Sano, H., and Horiuchi, S. (1997) Biochem. J. 322, 567-573). In the present study we examined the effects of insulin on macrophage scavenger receptor (MSR)-mediated endocytic uptake of AGE proteins. LECs expressing MSR showed an insulin-sensitive increase of endocytic uptake of AGE-bovine serum albumin (AGE-BSA). Next, RAW 264.7 cells expressing a high amount of MSR were overexpressed with human insulin receptor (HIR). Insulin caused a 3.7-fold increase in endocytic uptake of 125I-AGE-BSA by these cells. The effect of insulin was inhibited by wortmannin, a phosphatidylinositol-3-OH kinase (PI3 kinase) inhibitor. To examine at a molecular level the relationship between insulin signal and MSR function, Chinese hamster ovary (CHO) cells expressing a negligible level of MSR were cotransfected w...Continue Reading

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Citations

Jan 5, 2002·Diabetes/metabolism Research and Reviews·H Vlassara
May 15, 2010·Herz·Alin Stirban
Jan 6, 2007·Histochemistry and Cell Biology·Evanthia Diamanti-KandarakisAntoni J Duleba
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May 26, 2020·Life Sciences·Jing-Ling ZhuZhong-Cheng Mo

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