期刊文献+

小胶质细胞表型和功能的多样性与阿尔茨海默症 被引量:7

Role of diversity of phenotype and function of microglia on the pathogenesis of Alzheimer’s disease
暂未订购
导出
摘要 小胶质细胞(Microglia,MG)是中枢神经系统(Central nervous system,CNS)的固有免疫细胞,占CNS细胞的10%~15%。谱系追溯研究显示,小胶质细胞起源于红髓祖细胞,胚胎发育过程中,从卵黄囊迁移到大脑,并在脑实质筑巢、增殖。在CNS中,MG分为静息状态M0型和活化型M1、M2两种动态平衡状态。当受到外界有害物质刺激时,MG转化为M1表型,通过上调炎性通路并分泌大量的炎症因子、激活补体系统等对CNS造成损伤,而M2表型的MG通过分泌大量的抗炎因子和吞噬作用,能够清除毒性物质和抑制CNS疾病的发生。表明,MG在CNS中具有"双刃剑"的作用。本文简要综述了MG表型的多样性在补体系统、炎症通路、Tau蛋白磷酸化等发挥的作用,以及与AD关系的研究进展。 Microglia are intrinsic immune cells of the central nervous system(CNS),accounting for about 10%~15%of CNS cells.Pedigree retrospective studies have shown that microglia originate from erythroid progenitor cells.During embryonic development,microglia migrate from the yolk sac to the brain,nest and proliferate in the brain,and build nets and proliferate in the brain parenchyma.In CNS,microglia can be divided into static state M0 and activated state M1 and M2.When stimulated by harmful substances,microglia are transformed into M1-type,which causes damage to CNS by up-regulating inflammatory pathways,secreting a large number of inflammatory factors and activating the complement system,etc.,while M2-type microglia can clear toxic substances and inhibit the occurrence of CNS diseases by secreting large number of anti-inflammatory factors and phagocytosis.It shows that microglia has a"double-edged sword"effect in CNS.This paper briefly reviewed the role of microglia phenotypic diversity in complement system,inflammatory pathway,Tau phosphorylation,and its relationship with AD.
作者 国佳莹 石京山 Guo Jiaying;Shi Jingshan(Key Laboratory of Basic Pharmacology and Joint International Research Laboratory of Ethnomedicine of Ministry of Education,Zunyi Medical University,Zunyi Guizhou 563099,China)
出处 《合肥医科大学学报》 2020年第3期405-411,共7页 Journal of Zunyi Medical University
基金 国家自然科学基金资助项目(NO:U1812403)。
关键词 小胶质细胞 神经炎症 表型 阿尔茨海默病 microglia neuroinflammation phenotype Alzheimer’s disease
  • 相关文献

参考文献37

二级参考文献129

  • 1茅惠明,张伟英,金怡萍,汪浩,钱宪明.免疫印迹法检测老年白内障晶状体热休克蛋白27[J].现代检验医学杂志,2006,21(6):7-9. 被引量:1
  • 2戴志红,谢磊,赵耘.腺病毒的生物学特性[J].中国兽药杂志,2007,41(2):36-39. 被引量:6
  • 3Teich AF, Arancio O. Is the amyloid hypothesis of Alzheimer's disease therapeutically relevant [ J] ? Biochem J, 2012, 446 (2) : 165 - 177.
  • 4Mrak RE. Microglia in Alzheimer brain: a neuropathological perspective [J]. Int J Alzheimer's Dis, 2012, 2012: 165021.
  • 5Wyss-Coray T, Rogers J. Inflammation in Alzheimer disease-a brief re- view of the basic science and clinical literature[ J/OL]. Cold Spring Harb Perspect Med, 2012, 2(1) : a006346.
  • 6Aiyaz M, Lupton MK, Proitsi P, et al. Complement activation as a biomarker for Alzheimer' s disease [ J]. Immunobiology, 2012, 217 (2) : 204 -215.
  • 7Manthey HD, Woodruff TM, Taylor SM, et al. Complement compo- nent 5 a ( C5 a) [ J ]. Int J Biochem Cell Biol, 2009, 41 ( 11 ) : 2114 - 2117.
  • 8McGeer PL, McGeer EG. The possible role of complement activation in Alzheimer disease [ J]. Trends Mol Med, 2002, 8( 11 ): 519- 523.
  • 9Huberlang M, Sarma JV, Zetounes FS, et al. Generation of C5a in the absence of C3: a new complement activation pathway [ J ]. Nat Med, 2006, 12(6) : 682 -687.
  • 10Dahlgren KN, Manelli AM, Stine WB Jr, et al. Oligomeric and fibrillar species of amyloid-[3 peptides differentially affect neuronal vi- ability[J]. J Biol Chem, 2002, 277(35) : 32046 -32053.

共引文献211

同被引文献42

引证文献7

二级引证文献7

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部