Cited by 284Neuroinflammation and Neurodegeneration MechanismsAcute Ischemic Stroke ManagementIntracerebral and Subarachnoid Hemorrhage Research

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Macrophages prevent hemorrhagic infarct transformation in murine stroke models

Gliem, Michael, Mausberg, Anne Kathrin, Lee, John‐Ih, Simiantonakis, Ioannis, van Rooijen, Nico, Hartung, Hans‐Peter, Jander, Sebastian·2012·Annals of Neurology

DOI 10.1002/ana.23529

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Abstract

Objective: Inflammation is increasingly viewed as a new therapeutic target in subacute stages of brain infarction. However, apart from causing secondary damage, inflammation could equally promote beneficial lesion remodeling and repair. Distinct subpopulations of monocytes/macrophages (MOs/MPs) may critically determine the outcome of lesion‐associated inflammation. Methods: We addressed the role of bone marrow‐derived MOs/MPs in 2 different mouse models of ischemic stroke using a combined cell‐specific depletion, chemokine receptor knockout, bone marrow chimeric, and pharmacological approach. Results: Starting within 24 hours of stroke onset, immature Ly6c hi monocytes infiltrated into the infarct border zone and differentiated into mature Ly6c lo phagocytes within the lesion compartment. MO/MP infiltration was CCR2‐dependent, whereas we did not obtain evidence for additional recruitment via CX3CR1. Depletion of circulating MOs/MPs or selective targeting of CCR2 in bone marrow‐derived cells caused delayed clinical deterioration and hemorrhagic conversion of the infarctions. Bleeding frequently occurred around thin‐walled, dilated neovessels in the infarct border zone and was accompanied by decreased expression of transforming growth factor (TGF)‐β1 and collagen‐4, along with diminished activation of Smad2. Injection of TGF‐β1 into the lesion border zone greatly reduced infarct bleeding in MO/MP‐depleted mice. Interpretation: Bone marrow‐derived MOs/MPs recruited via CCR2 and acting via TGF‐β1 are essential for maintaining integrity of the neurovascular unit following brain ischemia. Future therapies should be aimed at enhancing physiological repair functions of CCR2+ MOs/MPs rather than blocking their hematogenous recruitment. ANN NEUROL 2012;71:743–752

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Authors: Gliem, M., Mausberg, A. K., Lee, J., Simiantonakis, I., van Rooijen, N., Hartung, H., & Jander, S.
Affiliations: Heinrich Heine University Düsseldorf (DE)
Corresponding author: Jander, Sebastian
ORCID: Gliem, Michael
Mausberg, Anne Kathrin
Lee, John‐Ih
Hartung, Hans‐Peter
Venue: Annals of Neurology
Publisher: Wiley
Published: 2012-06
Volume: 71
Issue: 6
Pages: 743-752
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.23529
OpenAlex: W2122031395
Cited by: 284
References: 39
Citations by year: 2026: 8 · 2025: 19 · 2024: 19 · 2023: 16 · 2022: 29 · 2021: 19 · 2020: 25 · 2019: 14 · 2018: 21 · 2017: 19 · 2016: 31 · 2015: 29 · 2014: 15 · 2013: 17 · 2012: 3
FWCI: 10.26
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 19 d)
Locations: Annals of Neurology (publishedVersion)
PubMed (publishedVersion)
Pure Amsterdam UMC (publishedVersion)
Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
Health Sciences › Medicine › Clinical Neurology › Intracerebral and Subarachnoid Hemorrhage Research
Keywords: macrophages, monocytes, ischemic stroke, hemorrhagic transformation, CCR2, TGF-β1, Smad2, neurovascular unit, infarct border zone, bone marrow-derived cells, cell depletion, CX3CR1
MeSH terms: CX3C Chemokine Receptor 1, CD68 Molecule, Animals, Antigens, Ly, Cell Differentiation, Diphtheria Toxin, Disease Models, Animal, Drug Administration Routes, Flow Cytometry, Gene Expression Regulation, Germanium, Interferon Inducers, Macrophages, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity, Organometallic Compounds, Propionates, Time Factors, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Leukocyte Common Antigens, Receptors, Chemokine, Infarction, Middle Cerebral Artery, Intracranial Hemorrhages, Brain Infarction, Stroke, Intracranial Thrombosis, Intercellular Signaling Peptides and Proteins, CD11b Antigen, Mice, Transforming Growth Factor beta1, Receptors, CCR2, Heparin-binding EGF-like Growth Factor

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Macrophages prevent hemorrhagic infarct transformation in murine stroke models

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