锌指蛋白基因抑制内皮细胞粘附分子表达及单核细胞粘附  

Overexpression of A20 inhibits OxLDL-inducible endothelial cells VCAM-1 expression and monocyte Adhesion

作　　者：柏力[1] 杨明璨[2] 李至伟 李小松[2] 李立[2] 张伟[2] 

机构地区：[1]成都军区昆明总医院急诊科 [2]第三军医大学基础医学部人体解剖学教研室 [3]解放军78511部队门诊部

出　　处：《局解手术学杂志》2010年第3期171-173,共3页Journal of Regional Anatomy and Operative Surgery

基　　金：国家自然科学基金资助项目(30770771)

摘　　要：目的单核细胞粘附是动脉粥样硬化发生的重要阶段,研究锌指蛋白A20基因在氧化型低密度脂蛋白诱导内皮细胞粘附分子表达及单核细胞粘附中的作用。方法脂质体DOTAP转染pEGFPEHA20-N1于原代培养的脐静脉内皮细胞,经G418筛选,A20表达经免疫荧光鉴定。激光共聚焦显微镜及微管吸吮系统分别检测转染前后氧化型低密度脂蛋白诱导单核细胞粘附情况及内皮细胞粘附分子VCAM-1表达。结果氧化型低密度脂蛋白能显著提高单核细胞粘附力及内皮细胞VCAM-1表达,A20基因能显著抑制氧化型低密度脂蛋白诱导单核细胞粘附及内皮细胞VCAM-1表达。结论A20基因对动脉粥样硬化的防治可能有一定作用。Objective To examine the effectiveness of A20 inhibits OxLDL-inducible endothelial cells VCAM-1 expression and monocyte adhesion.Methods With the help of DOTAP,endothelial cells were transfected with pEGFPEHA20-N1.The positive cell clones were selected with G418.Immunofluorescence analysis determined the stable transfection and expression of A20 in the endothelial cells.The expression of VCAM-1 in endothelial cells induction by OxLDL was determined by immunofluorescence and in situ hybridization.The adhension force between endothelial cells and monocytes was checked by micropipette aspiring system.Results A20 gene can significantly inhibit the VCAM-1 expression of endothelial cells and decrease the adhension force between endothelial cells and monocytes induction by OxLDL.Conclusion A20 gene can be helpful for the treatment atherosclerosis.

关 键 词：A20基因 氧化型低密度脂蛋白 VCAM-1 单核细胞 

分 类 号：R329.26[医药卫生—人体解剖和组织胚胎学] R543.5[医药卫生—基础医学]