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Cited by 342Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsAcute Ischemic Stroke Management

The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.

Proliferating Resident Microglia after Focal Cerebral Ischaemia in Mice

Denes, Adam, Vidyasagar, Rishma, Feng, Jianghua, Narvainen, Johanna, McColl, Barry W, Kauppinen, Risto A, Allan, Stuart M·2007·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1038/sj.jcbfm.9600495
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Abstract

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.

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Crossref · 10.1038/sj.jcbfm.9600495

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Research works printed but not linked: 2

  1. Kavec M, 2004, Proc Intl Soc Magn Res Med, 12, 133
  2. Schroeter M, 2006, Proc Int Soc Magn Reson Med, 14, 1459

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Metadata

Authors
Denes, A., Vidyasagar, R., Feng, J., Narvainen, J., McColl, B. W., Kauppinen, R. A., & Allan, S. M.
Affiliations
  • Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary
  • University of Birmingham (GB)
  • Chinese Academy of Sciences (CN)
  • Faculty of Life Sciences, Michael Smith Building, University of Manchester, Manchester, UK
  • University of Manchester (GB)
ORCID
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
2007-12
Volume
27
Issue
12
Pages
1941-1953
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1038/sj.jcbfm.9600495
OpenAlex
W2001952628
Cited by
342
References
40
Citations by year
2026: 4 · 2025: 3 · 2024: 9 · 2023: 17 · 2022: 17 · 2021: 36 · 2020: 14 · 2019: 22 · 2018: 27 · 2017: 17 · 2016: 33 · 2015: 23 · 2014: 18 · 2013: 28 · 2012: 19
FWCI
8.26
Type
journal article
Language
en
Open access
closed
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (publishedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
Keywords
microglial proliferation, focal cerebral ischemia, transient middle cerebral artery occlusion, blood-brain barrier disruption, neutrophil infiltration, macrophage infiltration, neuroinflammation, phagocytosis, neuroprotection, ischemic injury
MeSH terms
Animals, Antimetabolites, Bromodeoxyuridine, Ischemic Attack, Transient, Data Interpretation, Statistical, Dextrans, Fluorescent Antibody Technique, Iron, Macrophages, Magnetic Resonance Imaging, Male, Mice, Inbred C57BL, Monocytes, Oxides, Phagocytes, Microglia, Infarction, Middle Cerebral Artery, Neutrophil Infiltration, Cell Proliferation, Mice, Ferrosoferric Oxide, Magnetite Nanoparticles

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