Journal Article

DZNE-2026-00886

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png CX3CR1 Modulates Migration of Resident Microglia Towards Cortical Laser-Induced Lesions.

Wagner, J. (First author)DZNE* ; Antony, H. J.DZNE* ; Hoyer, C.DZNE* ; Lundgrén, K. ; Soliymani, R. ; Crux, S.DZNE* ; Justus, L. C.DZNE* ; Keppler, K.DZNE* ; Steffen, J.DZNE* ; Kurts, C. ; Engel, D. R. ; Herms, J.DZNE* ; Łałowski, M. ; Fuhrmann, M. (Last author)DZNE*

2026
Wiley-Liss Bognor Regis [u.a.]

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Please use a persistent id in citations: doi:10.1002/glia.70207

Abstract: Microglia are innate immune cells of the central nervous system (CNS). They extend their processes and migrate toward injuries in vivo. However, how the fractalkine receptor (CX3CR1) influences microglial migration remains unknown. Label-free proteomic profiling predicted changes in Ras homology family (RHO)-signaling activity that hint at dysregulated cytoskeleton signaling in Cx3cr1-deficient murine cortex tissue. To further investigate microglial migration, we carried out two-photon in vivo imaging at 4-h intervals for 72 h after a laser lesion in the cortex. Cx3cr1-deficient microglia showed enhanced migration toward the lesion. Additionally, the length and velocity of microglial fine processes extending toward the lesion were increased in Cx3cr1-deficient microglia. Migration remained unchanged in Ccr2-deficient mice, indicating that monocyte-derived macrophages/microglia did not contribute to microglia accumulation around the lesion. These results demonstrate that CX3CR1 modulates microglia migration toward laser-induced CNS injury. Manipulating microglia migration via the CX3CR1 signaling axis is therefore a potential target for the treatment of CNS injury.

Keyword(s): Animals (MeSH) ; Microglia: physiology (MeSH) ; Microglia: metabolism (MeSH) ; Microglia: pathology (MeSH) ; CX3C Chemokine Receptor 1 (MeSH) ; Cell Movement: physiology (MeSH) ; Cell Movement: genetics (MeSH) ; Cerebral Cortex: pathology (MeSH) ; Cerebral Cortex: injuries (MeSH) ; Cerebral Cortex: metabolism (MeSH) ; Receptors, Chemokine: genetics (MeSH) ; Receptors, Chemokine: metabolism (MeSH) ; Receptors, Chemokine: deficiency (MeSH) ; Lasers: adverse effects (MeSH) ; Receptors, CCR2: genetics (MeSH) ; Receptors, CCR2: metabolism (MeSH) ; Receptors, CCR2: deficiency (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice (MeSH) ; Mice, Knockout (MeSH) ; Mice, Transgenic (MeSH) ; Signal Transduction (MeSH) ; CX3CR1 ; cytoskeleton ; microglia ; migration ; CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Receptors, Chemokine ; Receptors, CCR2 ; Ccr2 protein, mouse

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Contributing Institute(s):

1. Neuroimmunology and Imaging (AG Fuhrmann)
2. Translational Brain Research (AG Herms)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2026

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DEAL Wiley ; Essential Science Indicators ; IF >= 5 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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