SUMO化修饰对高糖诱导的大鼠肾系膜细胞IκB/NF-κB信号的影响  

Effects of sumoylation on IκB / NF-κB signaling in the cultured rat glomerular mesangial cells induced by hyperglycomia

作　　者：黄炜[1] 徐玲[1] 徐勇[1] 周雪琴[1] 彭娟[1] 

机构地区：[1]泸州医学院附属医院内分泌科,四川泸州646000

出　　处：《基础医学与临床》2014年第12期1689-1693,共5页Basic and Clinical Medicine

基　　金：四川省教育厅科研项目(11ZB223)

摘　　要：目的探讨小泛素相关修饰物(SUMO)修饰对高糖诱导的肾系膜细胞IκB/NF-κB信号的影响。方法体外培养正常大鼠肾小球系膜细胞,设对照组、不同浓度高糖干预组和渗透压对照组,用免疫共沉淀检测SUMO1,SUMO2/3蛋白与IκBα蛋白的相互作用;免疫印迹检测IκBα、NF-κB P65蛋白表达。结果高糖特异性地减弱肾系膜细胞SUMO2/3与IκBα蛋白间的相互作用(P<0.05);高糖呈浓度-时间依赖性促进IκBα泛素化降解(P<0.05),同时上调NF-κB P65表达(P<0.05)。结论高糖特异性减弱IκBα的SUMO化修饰,可能介导了肾系膜细胞、NF-κB信号的激活,参与了糖尿病肾病的发病。Objective To investigate the effects of SUMOylation on IκB/NF-κB signaling in cultured rat mesangial cells induced by hyperglycomia. Methods Cultured HBZY-1 rat GMCs were divided into normal glucose group, high glucose groups, and osmotic control group. Interaction between SUMO1, SUMO2/3 and IκBα was examined by co-immunoprecipitation. The expression of IκBα , NF-κB P65 was measured by Western blot. Results The interaction between SUMO2/3 and IκBα in high glucose groups was significantly decreased as compared with normal glucose group （P 〈 0. 05 ）. IκBα in high glucose groups was degradated by ubiquitin-proteasome pathway in a dose and time-dependent manner（ P 〈 0. 05 ）, but the expression of NF-κB P65 increased （ P 〈 0. 05 ）. Conclusions High glucose level obviously changes the interaction between SUMO2/3 and IκBα in cultured rat GMCs, which may be involved in the activation of NF-κB by specifically impacting SUMOylation of IκBα .

关 键 词：SUMO化修饰 糖尿病肾病 IΚBΑ 

分 类 号：R587.2[医药卫生—内分泌]