抄録
A: Thermodynamic stability of disk–HDL was evaluated to be more stable than the starting mixture of free apoA–I and phosphatidylcholine (PC) large unilamellar vesicle (LUV). However, the rate of disk formation was very slow, suggesting the large kinetic barrier. Addition of sphingomyelin led to rapid microsolubilization of LUV and formation of the disk. Conformational change of apoA–I in acidic condition also resulted in progressive transformation of PC LUV to the disk. These findings raise the possibility that ABCA1 may act to lower the kinetic barrier and facilitate the disk–HDL generation. B: Cholesterol (Chol)–rich lipid emulsion (triolein–PC/Chol emulsion) was prepared as a model for chylomicron remnant. Internalization of the emulsion particles into macrophages induced leakage of lysosomal protease, cathepsin–L, to cytosol and cell death. This observation implied that Chol of chylomicron remnant plays a role in accelerating atherosclerosis.
