摘要
作者以^(125)I-标记的人VLDL和不含apo E的HDL_3为配体,研究了大鼠肝实质细胞(PC)及非肝实质细胞(NPC)的VLDL和HDL受体的生物学特性。结果显示:VLDL受体和HDL受体均可介导肝PC和NPC结合、摄取及降解相应的脂蛋白;肝NPC上该二受体的活性分别为PC的10倍和4倍;肝NPC上VLDL受体HDL受体的解离常数分别为15.0～34.2μg/ml和10.1～17.7μg/ml,最大结合容量分别为2170～2607ng/mg和1004～2738ng/mg细胞蛋白;VLDL受体活性受EDTA抑制及胆固醇的下降调节,HDL受体不受EDTA抑制但受胆固醇的上升调节。发现apoCⅢ对VLDL受体结合功能有明显抑制作用。
Saturable high-affinityVLDL and HDL receptor on parenchymalcells (PC). and non-parenchymal cells(NPC)freshly isolated from rat liver were studi-ed. The VLDL- and HDL-receptor couldmediate liver PC and NPC to bind,uptake,and degrade ^(125)I-labeled human VLDLand apoE-deficient HDL_3,and the activitiesof these two receptors(expressed as ng/mgcell protein) on NPC were about 10- and4-fold higher than those on PC,respective-ly. VLDL receptor on NPC with kd 15.0-84.2 μg/ml and Bmax 2170-2607 ng/mg cellprotein could be inhibited by EDTA. anddown-regulated by cell cholesterol content.HDL receptor on NPC with kd 10.1-17.7μg/ml and Bmax 1004-2738 ng/mg cell pro-tein could not be inhibited by EDTA, butcould be up-regulated by cell cholesterolcontent. Competitive inhibition assayshowed that VLDL r?ceptor could not onlybind VLDL and LDL, but also bind HDL_3to some extent. Unlabeled purified apolipo-protein CⅢ_(-1),, but apoAⅠ, CⅠ, CⅡ, couldeffectively inhibit ^(125)Ⅰ-labeled VLDL bind-ing to NPC. These results suggest that liverNPC may be more active than PC inclearing VLDL and HDL from circula-tion, and apolipoprotein CⅢ play animportant inhibitory role in these receptor-mediated processes.
出处
《华西医科大学学报》
CAS
CSCD
1991年第3期235-239,共5页
Journal of West China University of Medical Sciences
基金
国家攻关资助
关键词
肝细胞
脂蛋白受体
肝脏
Lipoprotein receptor
VLDL
HDL
Liver cells
Rat
