摘要
载脂蛋白AI促进胆固醇从外周细胞流出，在高密度脂蛋白对胆固醇的逆向运输中起关键作用。为探讨载脂蛋白AI介导胆固醇流出功能的结构特征，观察了天然存在的氨基酸置换：载脂蛋白AI结构中第156位上的缬氨酸由谷氨酸置换，和氨基酸缺失：第235位上的谷氨酸缺失对载脂蛋白AI促胆固醇从鼠腹腔巨噬细胞流出能力的影响。以体外培养的鼠腹腔巨噬细胞为对象，用氚标油酸酯标记的乙酰化低密度脂蛋白作泡沫细胞诱导物，巨噬细胞与载脂蛋白AI孵育一段时间后．测定由细胞释放入培养基中的3H标记胆固醇量。结果发现载脂蛋白AI结构中第156位的缬氨酸由谷氨酸置换不影响载脂蛋白AI的促细胞胆固醇流出能力，而第235位上的谷氨酸缺失可使胆固醇流出能力降低50％，差异有极显著性意义（P＜0．01）。此结果提示，载脂蛋白AI的C末端残基第235位谷氨酸对胆固醇流出功能起重要作用。
Aim The effects of replacement of amino acid residue Va1156 with Gln or deletion in Gln235 on the capacity of apolipoprotein AI(APo AI) to promote cholesterol efflux from murine peritoneal macrophages.Methods Cultured mouse peritoneal macrophages were used. 3 H-oleate labled acetyl low density lipoprotein (ac-LDL) was employed as an inducer for foam cell formation. After macrophages were cul-tured with Apo AI, 3 H-cholesterol released from cells to the medium was measured by scintillation spectrom-etry.Results The replacement of Va1156→Glu did not influence the capacity of Apo AI to promote cellular cholesterol efflux. However, a deletion in the residue Gln235 significantly reduced the ability of Apo AI to promote cellular cholesterol efflux.Conclusions Amino acid residue Glu235 of ApoAI is important for cellular cholesterol efflux.
出处
《中国动脉硬化杂志》
CAS
CSCD
1998年第3期202-205,共4页
Chinese Journal of Arteriosclerosis
基金
日中医学协会川医学金
关键词
载脂蛋白AI
胆固醇流出
鼠腹腔巨噬细胞
Apolipoprotein AI
Cholesterol ef-flux
Murine peritoneal macrophages
