Microglia in cerebral ischemia: molecular actions and interactions

被引:166
作者
Lai, AY
Todd, KG [1 ]
机构
[1] Univ Alberta, Neurochem Res Unit, Dept Psychiat, Edmonton, AB T6G 2R7, Canada
[2] Univ Alberta, Ctr Neurosci, Edmonton, AB T6G 2R7, Canada
关键词
microglia; cerebral ischemia; stroke; inflammation; cytokines; compliment factors; growth factors;
D O I
10.1139/y05-143
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The precise role of microglia in stroke and cerebral ischemia has been the subject of debate for a number of years. Microglia are capable of synthesizing numerous Soluble and membrane-bound biomolecules, some known to be neuroprotective, some neurotoxic, whereas others have less definitive bioactivities. The molecular mechanisms through which microglia activate these molecules have thus become an important area of ischemia research. Here we provide a survey review that summarizes the key actions of microglial factors in cerebral ischemia including complement proteins, chemokines, pro-inflarnmatory cytokines, neurotrophic factors, hormones, and proteinases, as well several important messenger molecules that play a part in how these factors respond to extracellular signals during ischemic injuries. We also provide some new perspectives on how microglial intracellular signaling may contribute to the seemingly contradictory roles of several microglial effector molecules.
引用
收藏
页码:49 / 59
页数:11
相关论文
共 123 条
  • [1] Early microglial reaction following mild forebrain ischemia induced by common carotid artery occlusion in rats
    Abrahám, H
    Lázár, G
    [J]. BRAIN RESEARCH, 2000, 862 (1-2) : 63 - 73
  • [2] Varied actions of proinflammatory cytokines on excitotoxic cell death in the rat central nervous system
    Allan, SM
    [J]. JOURNAL OF NEUROSCIENCE RESEARCH, 2002, 67 (04) : 428 - 434
  • [3] Differential matrix metalloproteinase expression in cases of multiple sclerosis and stroke
    Anthony, DC
    Ferguson, B
    Matyzak, MK
    Miller, KM
    Esiri, MM
    Perry, VH
    [J]. NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1997, 23 (05) : 406 - 415
  • [4] Tumor necrosis factor-alpha - A mediator of focal ischemic brain injury
    Barone, FC
    Arvin, B
    White, RF
    Miller, A
    Webb, CL
    Willette, RN
    Lysko, PG
    Feuerstein, GZ
    [J]. STROKE, 1997, 28 (06) : 1233 - 1244
  • [5] BRAIN-DERIVED NEUROTROPHIC FACTOR PROTECTS AGAINST ISCHEMIC CELL-DAMAGE IN RAT HIPPOCAMPUS
    BECK, T
    LINDHOLM, D
    CASTREN, E
    WREE, A
    [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1994, 14 (04) : 689 - 692
  • [6] Co-ordinated and cellular specific induction of the components of the IGF/IGFBP axis in the rat brain following hypoxic-ischemic injury
    Beilharz, EJ
    Russo, VC
    Butler, G
    Baker, NL
    Conner, B
    Sirimanne, ES
    Dragunow, M
    Werther, GA
    Gluckman, PD
    Williams, CE
    Scheepens, A
    [J]. MOLECULAR BRAIN RESEARCH, 1998, 59 (02): : 119 - 134
  • [7] Expression of IL-6 in the ischemic penumbra
    Block, F
    Peters, M
    Nolden-Koch, M
    [J]. NEUROREPORT, 2000, 11 (05) : 963 - 967
  • [8] Expression of TNF and TNF receptors (p55 and p75) in the rat brain after focal cerebral ischemia
    Botchkina, GI
    Meistrell, ME
    Botchkina, IL
    Tracey, KJ
    [J]. MOLECULAR MEDICINE, 1997, 3 (11) : 765 - 781
  • [9] Braun N, 1998, J NEUROSCI, V18, P4891
  • [10] Focal cerebral ischemia enhances glial expression of ecto-5'-nucleotidase
    Braun, N
    Lenz, C
    Gillardon, F
    Zimmermann, M
    Zimmermann, H
    [J]. BRAIN RESEARCH, 1997, 766 (1-2) : 213 - 226