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Alternatively activated brain-infiltrating macrophages facilitate recovery from collagenase-induced intracerebral hemorrhage

Alternatively activated brain-infiltrating macrophages facilitate recovery from collagenase-induced intracerebral hemorrhage
Min, H[Min, Hyunjung]Jang, YH[Jang, Yong Ho]Cho, IH[Cho, Ik-Hyun]Yu, SW[Yu, Seong-Woon]Lee, SJ[Lee, Sung Joong]
DGIST Authors
Yu, SW[Yu, Seong-Woon]
Issue Date
Molecular Brain, 9
Article Type
Animal CellAnimal ExperimentAnimal ModelAnimal TissueBioaccumulationBone Marrow Derived MacrophageBrain CellBrain DamageBrain HemorrhageBrain InjuryBrain ProtectionCell CountCell PolarityChemokine Receptor CX3CR1CocultureCollagenaseControlled StudyCX3CR1+ MacrophageDisease SeverityGlia CellHematomaImmune ResponseMacrophageMacrophage ActivationMacrophage FunctionMacrophage MigrationMacrophagesMaleMannose ReceptorMouseNeurologic DiseaseNon-HumanPhenotypePriority JournalProtein ExpressionWound Healing
Background: Intracerebral hemorrhage (ICH) is one of the major causes of stroke. After onset of ICH, massive infiltration of macrophages is detected in the peri-hematoma regions. Still, the function of these macrophages in ICH has not been completely elucidated. Results: In a collagenase-induced ICH model, CX3CR1+ macrophages accumulated in the peri-hematoma region. Characterization of these macrophages revealed expression of alternatively activated (M2) macrophage markers. In the macrophage-depleted mice, ICH-induced brain lesion volume was larger and neurological deficits were more severe compared to those of control mice, indicating a protective role of these macrophages in ICH. In the ICH-injured brain, mannose receptor-expressing macrophages increased at a delayed time point after ICH, indicating M2 polarization of the brain-infiltrating macrophages in the brain microenvironment. To explore this possibility, bone marrow-derived macrophages (BMDM) were co-cultured with mouse brain glial cells and then tested for activation phenotype. Upon co-culture with glia, the number of mannose receptor-positive M2 macrophages was significantly increased. Furthermore, treatment with glia-conditioned media increased the number of BMDM of M2 phenotype. Conclusions: In this study, our data suggest that brain-infiltrating macrophages after ICH are polarized to the M2 phenotype by brain glial cells and thereby contribute to recovery from ICH injury. © 2016 Min et al.
BioMed Central Ltd.
Related Researcher
  • Author Yu, Seong Woon Laboratory of Neuronal Cell Death
  • Research Interests Molecular mechanisms of neuronal cell death and neurodegeneration
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Department of Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles

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