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作 者:吴玉娟 曹镐禄[1] 何华宾[2] 罗煜 温军 郭哲 余常辉[4] 吴冰
机构地区:[1]赣南医学院基础医学院,江西赣州341000 [2]赣南医学院第一附属医院,江西赣州341000 [3]赣南医学院,江西赣州341000 [4]南方医科大学南方医院呼吸内科,广东广州510515
出 处:《赣南医学院学报》2017年第6期851-855,共5页JOURNAL OF GANNAN MEDICAL UNIVERSITY
基 金:国家自然科学基金项目(81560039);赣南医学院校级课题(YB201310)
摘 要:目的:探讨高迁移率族蛋白1(HMGB1)对成纤维样滑膜细胞(FLS)迁移的影响及线粒体分裂在其中的作用。方法:膝关节液分别取自RA患者(RA组)及正常人(normal组)。ELISA检测关节液中HMGB1水平。FLS分离自正常人膝关节滑膜组织,用膝关节液或者重组HMGB1刺激FLS,观察其迁移和线粒体分裂的变化。结果:RA组膝关节液中HMGB1水平较normal组明显升高,并且RA组膝关节液刺激的FLS细胞迁移和线粒体分裂较normal组明显增多。重组HMGB1可促进FLS细胞迁移及线粒体分裂。而线粒体分裂蛋白DRP1的抑制剂(Mdivi)可以抑制HMGB1诱导的线粒体分裂和FLS细胞迁移。结论:RA患者膝关节液中高水平的HMGB1可以通过诱导线粒体分裂促进成纤维样滑膜细胞迁移。Objective: To investigate the effects of high-mobility group protein B1(HMGB1) on migration of fibroblastlike synovial cells(FLS) and the role of mitochondrial fission in it.Methods: Knee joint fluid was taken from the knee joint of the RA patients(RA group) and the normal persons(normal group).HMGB1 levels of knee joint fluid were detected by ELISA.FLS were isolated from normal knee synovial membrane tissues.The migration and mitochondrial fission levels of FLS stimulated by knee joint fluid or recombinant HMGB1 were observed.Results: The HMGB1 level in knee joint fluid was obviously higher in RA group than that in normal group.Knee joint fluid from RA patients promoted migration and mitochondrial fission of FLS.Moreover,the FLS cell migration and mitochondrial fission stimulated by knee joint fluid were significantly increased in the RA group.Recombinant HMGB1 also accelerated migration and mitochondrial fission of FLS.Inhibitors of mitochondrial fission protein DRP1(Mdivi) inhibited the mitochondrial division and FLS cell migration induced by HMGB1.Conclusion: The high level of HMGB1 in knee joint fluid of RA patient could promote the migration of fibroblast-like synovial cells by inducing mitochondrial fission.
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