miR-128通过靶向p38调控树突细胞中IL-6的产生  

miR-128 Targets p38 to Regulate the Production of IL-6 in Dentritic Cell

作　　者：梁雪[1,2] 杨荣存[1] 

机构地区：[1]南开大学医学院,天津300071 [2]天津医科大学第二医院天津心脏病学研究所,天津300211

出　　处：《南开大学学报（自然科学版）》2014年第2期34-39,共6页Acta Scientiarum Naturalium Universitatis Nankaiensis

基　　金：国家自然科学基金重大研究计划(91029736)

摘　　要：p38 MAPK作为MAPK信号通路中关键的一类,对于树突细胞的成熟及激活等都具有至关重要的调节作用.首先利用生物信息学的方法预测了p38可能受到一系列microRNA的调控,进一步利用双荧光素酶报告载体系统证实了miR-128可直接作用于p38基因的3′非编码区域并抑制p38的表达.转染miR-128可以很显著地降低树突细胞中p38的蛋白水平,进而引起细胞因子IL-6分泌的减少.因此,利用miR-128可能是改善树突细胞抗肿瘤免疫治疗的一个新策略.p38 MAPK, a subgroup of MAPK signaling pathway, plays a critical role in modulating den- dritic cell maturation and activation. Combined with bioinformatics analysis, p38 was predicted as potential tar- get of series of micro RNAs. Using dual luciferase reporter assays, demonstrated that miR-128 could repress p38 expression by binding to the 3＇UTR of p38 in a direct and sequence-specific manner. Moreover, transfection of miR-128 mimics could significantly decrease the protein level of p38 in dendritic cell, and reasonably decrease cytokines IL-6 production. Thus, uncovered the potential role of miR-128 to improve immunotherapies against tumors.

关 键 词：miR-128 P38 MAPK 树突细胞 IL-6 

分 类 号：R392.1[医药卫生—免疫学]