Tags

Type your tag names separated by a space and hit enter

Proliferation of parenchymal microglia is the main source of microgliosis after ischaemic stroke.

Abstract

Stroke induces rapid activation and expansion of microglia, but the main source of microgliosis is controversial. Here we investigated the formation of microgliosis and infiltration of circulating cells in a photothrombosis stroke model by taking advantage of parabiosis and two-photon microscopy. We found that a small population of blood-derived CX3CR1(GFP/+) cells infiltrated the cerebral parenchyma, but these cells did not proliferate and were phenotypically distinguishable from resident microglia. CX3CR1(GFP/+) infiltrating cells also displayed different kinetics from reactive microglia. The number of CX3CR1(GFP/+) infiltrating cells peaked on Day 5 after stroke and then decreased. The decline of these infiltrating cells was associated with an active apoptotic process. In contrast, reactive microglia were recruited to the ischaemic area continuously during the first week after stroke induction. Immunohistology and in vivo two-photon imaging revealed that cells involved in the process of microgliosis were mainly derived from proliferating resident microglia. Expansion of microglia exhibited a consistent pattern and our in vivo data demonstrated for the first time that microglia underwent active division in regions surrounding the ischaemic core. Together, these results indicated that CX3CR1(GFP/+) infiltrating cells and reactive microglia represented two distinct populations of cells with different functions and therapeutic potentials for the treatment of stroke.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    School of Life Sciences, Lanzhou University, Lanzhou 73000, China.

    , , , ,

    Source

    Brain : a journal of neurology 136:Pt 12 2013 Dec pg 3578-88

    MeSH

    Animals
    Brain
    CX3C Chemokine Receptor 1
    Calcium-Binding Proteins
    Caspase 3
    Cell Proliferation
    Connective Tissue
    Disease Models, Animal
    Gene Expression Regulation
    Gliosis
    Green Fluorescent Proteins
    Mice
    Mice, Inbred C57BL
    Mice, Transgenic
    Microfilament Proteins
    Microglia
    Photic Stimulation
    Receptors, CCR2
    Receptors, Chemokine
    Stroke
    Time Factors

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    24154617

    Citation

    Li, Ting, et al. "Proliferation of Parenchymal Microglia Is the Main Source of Microgliosis After Ischaemic Stroke." Brain : a Journal of Neurology, vol. 136, no. Pt 12, 2013, pp. 3578-88.
    Li T, Pang S, Yu Y, et al. Proliferation of parenchymal microglia is the main source of microgliosis after ischaemic stroke. Brain. 2013;136(Pt 12):3578-88.
    Li, T., Pang, S., Yu, Y., Wu, X., Guo, J., & Zhang, S. (2013). Proliferation of parenchymal microglia is the main source of microgliosis after ischaemic stroke. Brain : a Journal of Neurology, 136(Pt 12), pp. 3578-88. doi:10.1093/brain/awt287.
    Li T, et al. Proliferation of Parenchymal Microglia Is the Main Source of Microgliosis After Ischaemic Stroke. Brain. 2013;136(Pt 12):3578-88. PubMed PMID: 24154617.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Proliferation of parenchymal microglia is the main source of microgliosis after ischaemic stroke. AU - Li,Ting, AU - Pang,Shengru, AU - Yu,Yongping, AU - Wu,Xiaoqian, AU - Guo,Jing, AU - Zhang,Shengxiang, Y1 - 2013/10/22/ PY - 2013/10/25/entrez PY - 2013/10/25/pubmed PY - 2014/2/11/medline KW - infiltrating cells KW - microglia KW - microgliosis KW - parabiosis KW - stroke SP - 3578 EP - 88 JF - Brain : a journal of neurology JO - Brain VL - 136 IS - Pt 12 N2 - Stroke induces rapid activation and expansion of microglia, but the main source of microgliosis is controversial. Here we investigated the formation of microgliosis and infiltration of circulating cells in a photothrombosis stroke model by taking advantage of parabiosis and two-photon microscopy. We found that a small population of blood-derived CX3CR1(GFP/+) cells infiltrated the cerebral parenchyma, but these cells did not proliferate and were phenotypically distinguishable from resident microglia. CX3CR1(GFP/+) infiltrating cells also displayed different kinetics from reactive microglia. The number of CX3CR1(GFP/+) infiltrating cells peaked on Day 5 after stroke and then decreased. The decline of these infiltrating cells was associated with an active apoptotic process. In contrast, reactive microglia were recruited to the ischaemic area continuously during the first week after stroke induction. Immunohistology and in vivo two-photon imaging revealed that cells involved in the process of microgliosis were mainly derived from proliferating resident microglia. Expansion of microglia exhibited a consistent pattern and our in vivo data demonstrated for the first time that microglia underwent active division in regions surrounding the ischaemic core. Together, these results indicated that CX3CR1(GFP/+) infiltrating cells and reactive microglia represented two distinct populations of cells with different functions and therapeutic potentials for the treatment of stroke. SN - 1460-2156 UR - https://www.unboundmedicine.com/medline/citation/24154617/Proliferation_of_parenchymal_microglia_is_the_main_source_of_microgliosis_after_ischaemic_stroke_ L2 - https://academic.oup.com/brain/article-lookup/doi/10.1093/brain/awt287 DB - PRIME DP - Unbound Medicine ER -