ArticleJournal of neuroinflammation2025
Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- ROS-responsive hydrogel delivering liposomal indole-3-propionic acid promotes spinal cord injury repair by enhancing CX3CL1-CX3CR1 mediated neuron-microglia communication.Materials today. Bio · 2026Article
- Targeting CX3CR1 Signaling Dynamics: A Critical Determinant in the Temporal Regulation of Post-Stroke Neurorepair.Brain sciences · 2025Review
- Evolving insights on the role of microglia in neuroinflammation, plasticity, and regeneration of the injured spinal cord.Frontiers in immunology · 2025Review
- Neuroinflammation: targeting microglia for neuroprotection and repair after spinal cord injury.Frontiers in immunology · 2025Review
- The role of microglial Tim-3 in neuroinflammation and functional recovery after spinal cord injury.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
backgroundRecent studies have confirmed the critical role of neonatal microglia in wound healing and axonal regeneration following spinal cord injury (SCI). However, the limited migration of microglia to the center of adult lesion may significantly impede their potential benefits.
methodsWe established a model of microglial centripetal migration and prolonged retention in C57BL/6J and transgenic mice by injecting exogenous C-X3-C motif chemokine ligand 1 (CX3CL1) and macrophage colony-stimulating factor (M-CSF) directly into the lesion site post-SCI. Wound healing and axonal preservation/regrowth was assessed anatomically, and kinematics analysis was conducted to determine the recovery of locomotor function.
resultsWe identified decreased expression and perilesional distribution of CX3CL1 as the primary reason for the limited centripetal migration of microglia. In situ injection of CX3CL1 into the lesion core promoted microglial centripetal migration, but alone did not improve functional recovery. Nevertheless, a combinational administration of CX3CL1 and M-CSF fostered both centripetal migration and prolonged retention of microglia, thereby effectively displacing blood-derived macrophage infiltration and optimizing wound healing and axonal preservation/regrowth after SCI. Notably, the beneficial effects of CX3CL1 and M-CSF co-administration were specifically blocked in C-X3-C motif chemokine receptor 1 (CX3CR1)-deficient mice. These phenomena may be related to the increase in spleen tyrosine kinase (SYK) levels, which boosts centripetal microglial phagocytosis.
conclusionOur study uncovers the criticality of microglial location and abundance in orchestrating SCI repair, highlighting centripetal microglial dynamics as valuable targets for therapeutic intervention.
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