血小板表面N糖β1,6-GlcNAc分支缺陷诱导骨髓源性巨噬细胞表型M1转化  

Defective N-glycanβ1,6-GlcNAc Platelets Promote M1 Phenotypic Switch in Polarization of Bone Marrow-Derived Macrophages

作　　者：蔡惠丽 邹雅倩 周蜜 王勃霏 易虹[1] 王树林 郭静明[1] Cai Huili;Zou Yaqian;Zhou Mi;Wang Bofei;Yi Hong;Wang Shulin;Guo Jingming(Department of Hematology,Yichang Central People's Hospital,The First College of Clinical Medical Science,China Three Gorges University&Institute of Hematology,China Three Gorges University,Yichang 443003,China;Department of Spinal Surgery,Yichang Central People's Hospital,The First College of Clinical Medical Science,China Three Gorges University,Yichang 443003,China)

机构地区：[1]三峡大学第一临床医学院[宜昌市中心人民医院]血液内科&三峡大学血液病研究所,湖北宜昌443003 [2]三峡大学第一临床医学院[宜昌市中心人民医院]脊柱外科,湖北宜昌443003

出　　处：《巴楚医学》2020年第4期6-10,共5页Bachu Medical Journal

基　　金：湖北省自然科学基金青年项目(No:2017CFB334);湖北省教育厅科学研究项目(No:B2017018);湖北省卫生和计划生育委员会科研项目(No:WJ2017M222)。

摘　　要：目的:探讨血小板N糖β1,6-GlcNAc分支缺陷对骨髓来源巨噬细胞(BMDMs)极化的影响。方法:通过苦马豆素灌胃动物模型获取N糖β1,6-GlcNAc分支缺陷血小板,流式细胞术检测血小板表面N糖β1,6-GlcNAc分支表达水平。将正常血小板和N糖支链缺陷血小板分别与BMDMs共同培养,采用流式细胞术、RT-PCR、ELISA等方法检测BMDMs的表型特征。结果:苦马豆素处理后的小鼠血小板N糖β1,6-GlcNAc表达较正常血小板明显减低(P<0.05)。与BMDMs共培养后,和正常血小板相比,N糖β1,6-GlcNAc分支缺陷血小板能够诱导巨噬细胞表达更多的诱导型一氧化氮合酶(iNOS)、CD16/32以及肿瘤坏死因子-ɑ(TNF-α),并降低CD206、Dectin-1、精氨酸酶-1(Arg-1)、白介素-10(IL-10)的表达。结论:N糖β1,6-GlcNAc分支缺陷血小板可在体外诱导BMDMs发生M1型极化,这可能是原发免疫性血小板减少症中免疫紊乱的发生机制之一。Objective:To investigate the effects of defective N-glycanβ1,6-GlcNAc branch on platelets during the differentiation of bone marrow-derived macrophages(BMDMs)in vivo.Methods:Platelets with defective N-glycanβ1,6-GlcNAc was obtained by swainsonine gavage,which was confirmed by flow cytometry.BMDMs were co-cultured with normal or abnormal platelets.Then the phenotype of BMDMs was determined by flow cytometry,RT-PCR and ELISA.Results:Platelets in swainsoine-treated mice expressed lower N-glycanβ1,6-GlcNAc branch compared with that in normal mice.After co-cultured with BMDMs,abnormal platelets produced increased inducible nitric oxide synthase(iNOS),CD16/CD32 and tumor necrosis factor(TNF-ɑ),while the expression of CD206,Dectin-1,Arg-1 and IL-10 were down-regulated,compared with normal control.Conclusion:N-glycanβ1,6-GlcNAc-defective platelets could induce the differentiation of BMDMs into proinflammatory M1 phenotype in vitro,which would be probably involved in pathogenesis of primary immune thrombocytopenia.

关 键 词：原发免疫性血小板减少症 N糖β1 6-GlcNAc分支 骨髓来源巨噬细胞 

分 类 号：R558[医药卫生—血液循环系统疾病]