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Proliferating resident microglia after focal cerebral ischaemia in mice.

Proliferating resident microglia after focal cerebral ischaemia in mice. Research Abstract Details 

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  • Proliferating resident microglia after focal cerebral ischaemia in mice. Abstract Text:

    adam denesAdam Denes,rishma vidyasagarRishma Vidyasagar,jianghua fengJianghua Feng,johanna narvainenJohanna Narvainen,barry w mccollBarry W McColl,risto a kauppinenRisto A Kauppinen,stuart m allanStuart M Allan,adam denesAdam Denes,rishma vidyasagarRishma Vidyasagar,jianghua fengJianghua Feng,johanna narvainenJohanna Narvainen,barry w mccollBarry W McColl,risto a kauppinenRisto A Kauppinen,stuart m allanStuart M Allan,

    Cerebral ischaemia usually results in the rapid death of neurons within the immediate territory of the affected artery. Neuronal loss is accompanied by a sequence of events, including brain oedema, blood-brain barrier (BBB) breakdown, and neuroinflammation, all of which contribute to further neuronal death. Although the role of macrophages and mononuclear phagocytes in the expansion of ischaemic injury has been widely studied, the relative contribution of these cells, either of exogenous or intrinsic central nervous system (CNS) origin is still not entirely clear. The purpose of this study, therefore, was to use different durations of transient middle cerebral artery occlusion (tMCAo) in the mouse to investigate fully post-occlusion BBB permeability and cellular changes in the brain during the 72 h post-MCAo period. This was achieved using in vivo magnetic resonance imaging (MRI) and cell labelling techniques. Our results show that BBB breakdown and formation of the primary ischaemic damage after tMCAo is not associated with significant infiltration of neutrophils, although more are observed with longer periods of MCAo. In addition, we observe very few infiltrating exogenous macrophages over a 72 h period after 30 or 60 mins of occlusion, instead a profound increase in proliferating resident microglia cells was observed. Interestingly, the more severe injury associated with 60 mins of MCAo leads to a markedly reduced proliferation of resident microglial cells, suggesting that these cells may play a protective function, possibly through phagocytosis of infiltrating neutrophils. These data further support possible beneficial actions of microglial cells in the injured brain.

    Proliferating resident microglia after focal cerebral ischaemia in mice. Publishing Authors By Initials

    a denesA Denes,r vidyasagarR Vidyasagar,j fengJ Feng,j narvainenJ Narvainen,bw mccollBW McColl,ra kauppinenRA Kauppinen,sm allanSM Allan,a denesA Denes,r vidyasagarR Vidyasagar,j fengJ Feng,j narvainenJ Narvainen,bw mccollBW McColl,ra kauppinenRA Kauppinen,sm allanSM Allan,

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    Proliferating resident microglia after focal cerebral ischaemia in mice. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of cerebral blood flow and metabolism : of

    VOLUME: 27

    Page Numbers: 1941-53

    Journal Abbreviation: J. Cereb. Blood Flow Metab.

    ISSN: 0271-678X

    DAY: 18

    MONTH: 04

    YEAR: 2007

    Proliferating resident microglia after focal cerebral ischaemia in mice. Information

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    LANGUAGE: eng

    NlmUniqueID: 8112566

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    Grant and Affiliation Information for Proliferating resident microglia after focal cerebral ischaemia in mice.

    AFFILIATION: Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary. denesa@koki.hu

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Cereb Blood Flow Metab

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