摘要
目的 探讨具有神经元特性的神经母细胞瘤细胞在急性缺氧后不协调类33磷蛋白1（Ulip1）与缺氧诱导因子-1α（HIF-1α）表达水平的变化.方法 选择具有神经元特性的神经母细胞瘤细胞株KCNR和BE2,将细胞分别置于正常氧浓度（体积分数为20%O2）和缺氧条件下（1%O2）处理4 h,提取蛋白.采用蛋白质免疫印迹法（Western blotting）定量测定Ulip1和HIF-1α表达.结果 在KCNR和BE2细胞急性缺氧4 h后,HIF-1α表达水平均显著升高,Ulip1的两个异构体Ulip1a和Ulip1b表达水平均降低;其中HIF-1α表达水平在KCNR细胞内升高了1.6倍,在BE2细胞内升高了2.9倍;Ulip1a在KCNR细胞内降低了55%,在BE2细胞内降低了20%;Ulip1b在KCNR细胞内降低了44%,在BE2细胞内降低了13%.结论 Ulip1可能通过影响HIF-1α参与了缺氧诱导的神经细胞损伤及之后的修复过程.
Objective To study the differences in expression of uncoordinated 33-like phosphoprotein 1 （Ulip1） and hypoxia-inducible factor-1α （HIF-1α） in neuroblastoma cell lines that have neuronal characteristics under normoxia and hypoxia conditions. Methods Two neuroblastoma cell lines （KCNR and BE2） which had neuronal characteristics were used in this study. The neuroblastoma cells were cultured under normoxic （20% of oxygen） or hypoxic （1% of oxygen） conditions for 4 hours, then cells were harvested and proteins were extracted. Western blotting was used to detect the levels of Ulipl and HIF-1α.Results After 4-hour hypoxia treatment, the expression of HIF-1α increased significantly in both cell lines,while the expression of Ulip1a and Ulip1b, which were two isoforms of Ulip1, decreased. There was an 1.6-fold increase of HIF-1α expression in KCNR cells and 2. 9-fold increase in BE2 cells; for Ulip1a expression, there was a 55% decrease in KCNR cells and a 20% decrease in BE2 cells; for Ulip1b expression, there was a 44% decrease in KCNR cells and a 13% decrease in BE2 cells. Conclusion Ulip1 maybe involved in the hypoxia-induced damage or repair processes in neuronal cells through HIF-1α.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2010年第10期614-616,共3页
Chinese Critical Care Medicine
基金
基金项目：辽宁省科研计划项目（2009225010-12）
