摘要
目的:晚期糖基化终产物受体(RAGE)与其配体结合在炎症及免疫反应中具有重要作用。本研究探讨内质网应激(ERS)在高迁移率族蛋白B1(HMGB1)诱导树突状细胞(DC)表面RAGE上调中的作用及意义。方法:分离正常BALB/c小鼠脾脏DC进行体外培养,给予HMGB1刺激后检测DC表面RAGE表达水平及细胞ERS相关分子表达/活化水平。另外,给予不同剂量ERS特异性诱导剂衣霉素(0.1、1、10μg/ml)刺激24、48、72 h,检测DC表面RAGE表达情况。结果:HMGBl刺激诱导DC中ERS相关分子表达/活化水平明显上调(P<0.05),细胞表面RAGE表达水平也明显上调;衣霉素刺激亦可诱导DC表面RAGE表达增强,且呈一定的时间依赖性,刺激时间越长,RAGE表达水平越高。结论:DC表面RAGE表达水平升高与ERS反应密切相关。
Objective： To clarify the involvement of endoplasmic reticulum stress （ERS） in up-regulation of receptor for advanced glycation endproduets （RAGE） on surface of dendritic cells （IX;） induced by high mobility group box-1 protein （HMGB1）. Methods：DCs were isolated from the spleens of male BALB/c mice. Expressions of ERS related molecules were analyzed by Western blot analysis, and the expression of RAGE on surface of DC was determined by flow cytometry after HMGB1 stimulation. The effect of tunicamycin （0. 1,1,10 μg/ml for 24, 48,72 hours） on RAGE expression was also assessed by flow cytometry. Results： HMGB1 induced up-regulation of RAGE expression and significant ERS response in murine splenic DCs. Pharmacological ERS （induced by tunicamycin） resulted in enhanced expression of RAGE on surface of DCs. Conclusions： These results indicate that ERS is crucial for up-regulation of RAGE on surface of DCs.
出处
《感染．炎症．修复》
2011年第4期197-201,共5页
Infection Inflammation Repair
基金
国家自然科学基金项目(81071545
30800437
81130035
81121004)
国家重点基础研究发展计划项目(2012CB518102)
创伤
烧伤与复合伤国家重点实验室开放课题(SKLKF201103
SKLKF201002)
关键词
脓毒症
树突状细胞
晚期糖基化终产物受体
内质网应激
Sepsis Dendritic ceils Receptor for advanced glycation endproducts Endopiasmie reticulum stress
