人CD59突变促进糖尿病血管并发症发生  

Mutation of human CD59 accelerates occurrence of human diabetic vascular proliferative complications

作　　者：张丽[1] 高美华[1] 

机构地区：[1]青岛大学医学院免疫学教研室

出　　处：《免疫学杂志》2009年第6期693-696,共4页Immunological Journal

基　　金：国家自然基金资助项目(30170893)

摘　　要：目的证实人CD59突变抗补体活性下降,促进糖尿病血管并发症的发生发展。方法构建2种HMCD59重组质粒,转染CHO细胞;FCM筛选高表达细胞,荧光免疫测定和固相酶免疫测定加一步检测阳性细胞。糖化培养阳性细胞,BCECF染料释放试验比较糖化人突变CD59和糖化人正常CD59抗补体活性。ELISA测定30例糖尿病无血管病变组和30例Ⅱ型糖尿病血管病组血清PDGF、bFGF含量。结果筛选细胞株表达率分别为59.8%、53.0%、54.5%;BCECF染料释放试验显示糖化后人突变CD59细胞比较糖化前染料释放率高(P<0.01);而正常CD59细胞较糖化后细胞染料释放率差异不明显(P>0.05)。Ⅱ型糖尿病有血管病变组与糖尿病无血管病变组相比,血清PDGF、bFGF明显增高(P<0.01)。结论证实人CD59突变后易糖化抗补体活性下降加速糖尿病血管病的发生发展。Objective To confirm gene mutation of human complement regulatory protein CD59 accelerates occurrence of the vascular proliferative complication of human diabetes. Methods The recombinant pALTER-MAX plasmids containing respective human gene mutant CD59 cDNA and pcDNA were co-transfected into CHO cell by cation lipoid mediating method. Highly expressing cells were selected by flow cytometry,immunofluorescence technique,and immunohistochemistry technique. These cells were cultivated in high glucose,and the fu...

关 键 词：CD59 真核表达 糖化 补体 免疫分子 

分 类 号：R392[医药卫生—免疫学]