Journal of Glycomics & Lipidomics
Open Access
ISSN: 2153-0637
+44 1223 790975
ISSN: 2153-0637
+44 1223 790975
Itsuko Ishii
Chiba University Hospital, Japan
Posters-Accepted Abstracts: J Glycomics Lipidomics
Macrophage foam cell formation is hallmark of atherosclerosis. Acrolein is highly reactive alpha, beta-unsaturated aldehyde produced by polyamine oxidation following cell damage endogenously. Acrolein could conjugate to protein and generate acrolein-lysine adducts and intra- or extra- molecular cross-links. It has been reported that acrolein-lysine adducts were detected in human atherosclerotic lesions. Furthermore protein conjugated acrolein detected in human LDL. These finding suggests that acrolein may contribute to macrophage foam cell formation and atherogenesis through modification of LDL. The purpose of this study is whether acrolein-conjugated LDL (Acro-LDL) induces macrophages to foam cells. Acro-LDL was prepared by incubation of LDL and acrolein. The mobilities of Acro-LDL in agarose gel electrophoresis were increased by modification with acrolein, and there were dose-dependent manner of acrolein concentration used in modification. Acro- LDL induced higher cholesterol accumulation in macrophages derived from THP-1 cells than LDL and oxidized LDL. Antiscavenger receptor class A type 1 (SR-A1) antibody inhibited uptake of Acro-LDL by macrophages derived from THP-1. Apolipoprotein B in Acro-LDL reacted with antibody for modified lysine, the molecular weight changed higher, and resisted to be hydrolyzed by lysosomal enzyme. Acidic cholesterol esterase and acyl-Coenzyme A: cholesterol acyltransferase activity was statistically increased in macrophages treated with Acro-LDL, but neutral cholesterol esterase activity did not change, resulting increase cholesteryl ester. It is concluded that macrophages are converted to foam cells by Acro-LDL via SR-A1 pathway.
Email: iishii@faculty.chiba-u.jp