摘要
目的 探讨转化生长因子β1(TGF β1)对巨噬细胞清道夫受体 A(ScR A)的影响。 方法 利用鼠单克隆抗人TGF β1抗体 (AntiTGF β1Ab) ,细胞培养 ,受体摄取配体及Northernblot印迹方法 ,观察AntiTGF β1Ab对人类单核细胞株 (THP 1细胞 )由来巨噬细胞受体摄取乙酰化LDL(Ac LDL)以及对ScR AmRNA表达的影响。结果 巨噬细胞对Ac LDL的摄取随AntiTGF β1Ab浓度的增加而增加。Ac LDL结合量 (ng mgprotein)与对照组 (36 89± 1 31)比较 ,投用 1 0、3 0 μg mlAntiTGF β1Ab ,其Ac LDL结合量分别为 45 5 6± 0 81(P <0 0 5 ) ,6 0 94± 1 17(P <0 0 1)。摄入量 (ng mgprotein)与对照组 (35 0 5 9± 6 0 3)比较 ,分别为 40 3 48± 4 37(P <0 0 5 ) ,5 0 3 6 1± 11 77(P <0 0 1)。降解量 (ng mgprotein)与对照组 (1382 0 6± 3 0 9)比较 ,分别为 16 17 71± 39 0 8,1934 84± 42 6 7(P<0 0 1)。巨噬细胞ScR AmRNA表达随AntiTGF β1Ab浓度的增加而增强。与空白对照组比较 ,投用 1 0、3 0 μg mlAntiTGF β1Ab ,其ScR AmRNA表达分别增强 15 7%和 38 2 %。结论 TGF β1抑制THP 1细胞由来巨噬细胞ScR A的表达。TGF
Objective To investigate whether transforming growth factor-β1(TGF-β1) can influence macrophage scavenger receptor class A type Ⅰ and type Ⅱ (ScR-A).Methods TPA were differentiated from 12-O-tetradecanoylphobol-13-acetate-treated THP-1 monocytes.Macrophages with different concentrations of mouse monoclonal anti-human TGF-β1 antibody (Anti TGF-β1 Ab),their uptake of acetylated low density lipoprotein (Ac-LDL)(including 4℃ binding,37℃ uptake and degradation) and ScR-A mRNA expression were measured.Results Pretreatment with 1.0 to 3.0 μg/ml of Anti TGF-β1 Ab significantly increased Ac-LDL binding,uptake,and degradation.ScR-A mRNA expression in the macrophages was also enhanced by treatment with Anti TGF-β1 Ab.Conclusions TGF-β1 can inhibit ScR-A expression in macrophages derived from THP-1 monocytes and this effect may be involved in atherogenesis and atherosclerosis.
出处
《中华老年心脑血管病杂志》
CAS
2001年第4期257-259,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
辽宁省博士启动基金资助项目 (9710 10 )
辽宁省教育厅专项资助项目 (2 0 12 2 163 )
关键词
转化生长因子Β1
巨噬细胞
清道夫受体-A
动脉粥样硬化
transforming growth factor-β1
macrophage scavenger receptor class A type Ⅰ and type Ⅱ
atherosclerosis
