脂蛋白(a)对巨噬细胞清道夫受体-A表达的影响

被引:10
作者
安君
闫德民
谷春久
机构
[1] 中国医科大学第一临床学院心脏外科
[2] 中国医科大学第一临床学院心脏外科 沈阳
[3] 沈阳
关键词
脂蛋白(a); 巨噬细胞;
D O I
暂无
中图分类号
R392.1 [免疫生物学];
学科分类号
100102 ;
摘要
目的 研究脂蛋白 (a) [lipoprotein(a) ,Lp(a) ]对巨噬细胞清道夫受体A(scavengerreceptorclassAtypeIandtypeII,ScR A)的影响。方法 利用细胞培养、受体摄取配体及Northern印迹杂交方法 ,观察Lp(a)对从人类单核细胞株细胞形成的巨噬细胞受体摄取乙酰化LDL (acetylatedLDL ,Ac LDL)以及对THP 1细胞形成的巨噬细胞ScR AmRNA表达的影响。结果 人类单核细胞株细胞形成的巨噬细胞对Ac LDL的结合量随Lp(a)浓度的增加而增加 ,而天然LDL对此无影响。加入 5 0μg/mlLp(a) ,巨噬细胞对Ac LDL结合量为 ( 188 0 6± 16 80 )ng/mg蛋白 ,与对照组的 ( 4 8 2 6± 5 61)ng/mg蛋白比较显著增加 (P <0 0 1) ;巨噬细胞对Ac LDL的摄入量为 ( 3 63 80± 11 77)ng/mg蛋白 ,与对照组的 ( 2 2 8 15± 17 0 7)ng/mg蛋白比较显著增加 (P <0 0 5 ) ;巨噬细胞对Ac LDL的降解量为( 94 8 17± 3 1 43 )ng/mg蛋白与对照组的 ( 60 8 68± 3 8 11)ng/mg蛋白比较显著增加 (P <0 0 5 )。加入5 0 μg/mlLp(a) ,其ScR AmRNA表达明显增强 ,与对照组比较增强 4 3 5 6%。 结论 Lp(a)可增强从THP 1细胞形成的巨噬细胞ScR A基因的表达 ,Lp(a)的这种作用可能参与了动脉粥样硬化形成和发展的病理过程。
引用
收藏
页码:44 / 47
页数:4
相关论文
共 12 条
[1]  
The metabolism of very low density lipoprotein protein.I. Preliminary in vitro and in vivo observation. Bilheimer DW,Eisenberg S,Levy RI. Biochimica et Biophysica Acta . 1972
[2]  
Degradation of cationized low density lipoprotein and regulation of cholesterol metabolism in homozygous familial hypercholesterolemia fibroblasts. Basu SK,Goldstein JL,Anderson GW,et al. Proceedings of the National Academy of Sciences of the United States of America . 1976
[3]  
Atherosclerosis[P]. DONG CHUNMING;GOLDSCHMIDT PASCAL J.中国专利:US2008095751A1,2008-04-24
[4]  
Insolublecomplexformationoflipoprotein(a)withlowdensitylipoproteininthepresenceofcalciumions. YashiroA ,,O′NeilJ,HoffHF. Journal of Biochemistry . 1993
[5]  
The mysteries of Lp (a) lipoprotein. Utermann G. Science . 1990
[6]  
Lipoprotein (a): intrigues and insights. Hobbs HH,White AL. Current Opinion in Lipidology . 1999
[7]  
Lipoprotein(a) and inflammation in human coronary atheroma: association with the severity of clinical presentation. Dangas G,Mehran R,Harpel P,et al. Journal of the American College of Cardiology . 1998
[8]  
Acquisition of secretion of transforming growth factor-beta 1 leads to autonomous suppression of scavenger receptor activity in a monocyte-macrophage cell line, THP-1. Nishimura N,Harada-shiba M,Tajima S,et al. Journal of Biological Chemistry . 1998
[9]  
The atherogenec lipoprotein(a) is internalized and degraded in a process mediated by the VLDL receptor. Argraves KM,Kozarsky KF,Fallon JT,et al. The Journal of Clinical Investigation . 1997
[10]  
Malodialdehyde modification of lipoprotein(a) produces avid uptake by human monocytemacrophages. Haberland ME,Fless GM,Scanu AM,et al. Journal of Biological Chemistry . 1992