Wiklund O, Carew T E, Steinberg D
Arteriosclerosis. 1985 Mar-Apr;5(2):135-41. doi: 10.1161/01.atv.5.2.135.
The present study was designed to determine whether binding of low density lipoprotein (LDL) to endothelial LDL receptors contributes significantly to the penetration of LDL into the normal rabbit aorta. Initial flux rate was used as a measure of uptake of LDL. Reductive methylation of LDL is known to block its recognition by the LDL receptor. Therefore, the difference in flux rates of native LDL and reductively methylated LDL (methyl-LDL) was assumed to represent the receptor-dependent uptake. Native LDL and methyl-LDL were labeled with different isotopes (125I or 131I) and both were injected simultaneously into the same rabbit. After 30 to 60 minutes, trichloroacetic acid-precipitable counts were determined in aortic specimens. The initial flux rates, expressed as plasma clearance (nl/g/hr), were 1787 for native LDL and 1924 for methyl-LDL. The difference was not significant, which suggests that the flux of LDL into the aorta is not significantly dependent upon, or regulated by, endothelial LDL receptors, but is mediated by other mechanisms.
本研究旨在确定低密度脂蛋白（LDL）与内皮LDL受体的结合是否对LDL渗透进入正常兔主动脉有显著作用。初始通量率用作LDL摄取的指标。已知LDL的还原甲基化会阻止其被LDL受体识别。因此，天然LDL和还原甲基化LDL（甲基化LDL）通量率的差异被认为代表受体依赖性摄取。天然LDL和甲基化LDL用不同的同位素（125I或131I）标记，并且将两者同时注射到同一只兔子体内。30至60分钟后，测定主动脉标本中三氯乙酸可沉淀计数。以血浆清除率（nl/g/hr）表示的初始通量率，天然LDL为1787，甲基化LDL为1924。差异不显著，这表明LDL进入主动脉的通量并非显著依赖于或受内皮LDL受体调节，而是由其他机制介导。
