载脂蛋白C3诱导的内皮细胞ZO-1的表达  

The regulation of ZO-1 induced by APOC3 in endothelial cells

作　　者：俞娟[1,2] 陶赟[1] 戴璐 熊怡淞[3] 王旭东[1] 景蓉蓉[1] 季伙燕[1] 王惠民[1] 仲人前[4] 

机构地区：[1]南通大学附属医院检验医学中心,南通226001 [2]南通大学公共卫生学院,南通226001 [3]成都军区总医院检验科,成都610083 [4]第二军医大学附属长征医院实验诊断科全军临床免疫中心,上海200003

出　　处：《现代免疫学》2017年第6期478-484,共7页Current Immunology

基　　金：国家自然科学基金(81301484;81302596)

摘　　要：研究载脂蛋白C3对内皮细胞紧密连接中ZO-1表达的作用。采用细胞培养的方法,通过qRT-PCR、免疫荧光、流式细胞术、Western blotting等技术检测APOC3作用状态下内皮细胞内相关分子ZO-1的表达。结果显示,APOC3通过TNF-α引起血管内皮紧密连接中重要蛋白ZO-1表达上升,NF-κB也参与其中,引起内皮功能紊乱。这说明抑制APOC3引起的ZO-1表达改变有可能成为心血管疾病的一个新的治疗思路与靶点。To investigate the effects of APOC3 on the expression of ZO-1 in the tight junction of endothelial cells,the HUVECs were cultured with APOC3,and the expression of ZO-1 in the endothelial cells was detected by real-time fluorescence quantitative PCR,immunofluorescence,flow cytometry and Western blotting.The results showed that APOC3 induced the change of expression of ZO-1 and proliferation of cells through TNF-α.NF-κB also took part in this process and induced endothelial dysfunction.We concluded that the inhibition of ZO-1 expression induced by APOC3 could be a new way to treat the CVDs.

关 键 词：载脂蛋白C3 内皮功能紊乱 ZO-1 炎症 

分 类 号：R392.11[医药卫生—免疫学]