高糖对肾小球系膜细胞ERK1／2蛋白表达泛素化调节的影响  

The effect of high glucose on the expression of ERK1/2 in glomerular mesangial cells via ubiquitin-proteasome pathway

作　　者：杨军[1] 马红艳[1] 徐玲[1] 徐勇[1] 

机构地区：[1]泸州医学院附属医院内分泌科,四川646000

出　　处：《中国糖尿病杂志》2011年第1期34-36,共3页Chinese Journal of Diabetes

基　　金：国家自然科学基金资助项目(30670980);四川省杰出青年基金项目(08ZQ026-026)

摘　　要：目的探讨高糖作用的肾小球系膜细胞ERK1/2蛋白表达与泛素-蛋白酶体调节途径的关系。方法体外培养大鼠肾小球系膜细胞,将高糖作为刺激因子,特异性泛素蛋白酶体抑制剂MG132作为干预因素。用蛋白免疫印迹法检测各组系膜细胞ERK1/2的表达,细胞免疫荧光染色及激光共聚焦显微镜检测各组系膜细胞ERK1/2的表达、转位。结果高糖组系膜细胞ERK1/2表达较正常血糖组均增多(P<0.05),还可促进ERK1/2由胞浆向胞核内激活、转位,高糖组加入MG132后,系膜细胞ERK1/2表达和激活、转位均减弱(P<0.05)。结论高糖可通过泛素蛋白酶体途径诱导肾系膜细胞ERK1/2表达增强和ERK1/2由胞浆向胞核内激活、转位。Objective To explore the relationship betweea ubiquitin-proteasome pathway（UPP） and ERK1/2 in cultured rat glomerular mesangial cells. Methods The cultured HBZY-1 ratglomerular mesangial cells were stimulated by high glucose, MG132 as an inhibitor of UPP was used to act on the cells. The expression of ERK1/2 were measured by Western-blotting assay, and the activation of ERK1/2 were measured by immunofluorescence and laser scanning confocal microscope. Results Compared with normal glucose group, the values of ERK1/2 expression, activation and transposition from endochylema to nucleus were increased in high glucose groups. The expression of ERK1/2 in high glucose groups were decreased obviously after adding MG132 （P〈0.05）. Conclusions High glucose can significantly increase the expression of ERK1/2 via the UPP and its activation and transposition from endoehylema to nucleus.

关 键 词：糖尿病肾病 肾小球系膜细胞 泛素-蛋白酶体途径 ERK1/2 

分 类 号：R587.2[医药卫生—内分泌] R692[医药卫生—内科学]