ArticleNeural regeneration research2023
Macrophage migration inhibitory factor facilitates astrocytic production of the CCL2 chemokine following spinal cord injury.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Enhanced MIF/CD74 axis activity shapes B cell functioning following traumatic spinal cord injury.Journal of neuroinflammation · 2026Article
- GPX4 activator enhances neuroprotection and functional recovery in spinal cord injury.Journal of orthopaedic translation · 2025Article
- Article
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- Controlled release of MIF siRNA and GDNF protein from a photocurable scaffold efficiently repairs spinal cord injury.MedComm · 2025Article
- Usp18 Mediates D-Dopachrome Tautomerase-Induced Astrocytic Inflammation After Spinal Cord Injury.Journal of inflammation research · 2025Article
- Lentivirus-mediated Knockdown of Ski Improves Neurological Function After Spinal Cord Injury in Rats.Neurochemical research · 2024Article
- Biomineralized MnOPharmaceutics · 2024Article
- Identification of key autophagy-related genes and pathways in spinal cord injury.Scientific reports · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation. Overproduced chemokines are responsible for the migratory process of the leukocytes, but the regulatory mechanism underlying the production of chemokines from resident cells of the spinal cord has not been fully elucidated. We examined the protein levels of macrophage migration inhibitory factor and chemokine C-C motif chemokine ligand 2 in a spinal cord contusion model at different time points following spinal cord injury. The elevation of macrophage migration inhibitory factor at the lesion site coincided with the increase of chemokine C-C motif chemokine ligand 2 abundance in astrocytes. Stimulation of primary cultured astrocytes with different concentrations of macrophage migration inhibitory factor recombinant protein induced chemokine C-C motif chemokine ligand 2 production from the cells, and the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine attenuated the stimulatory effect. Further investigation into the underlying mechanism on macrophage migration inhibitory factor-mediated astrocytic production of chemokine C-C motif chemokine ligand 2 revealed that macrophage migration inhibitory factor activated intracellular JNK signaling through binding with CD74 receptor. Administration of the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine following spinal cord injury resulted in the reduction of chemokine C-C motif chemokine ligand 2-recruited microglia/macrophages at the lesion site and remarkably improved the hindlimb locomotor function of rats. Our results have provided insights into the functions of astrocyte-activated chemokines in the recruitment of leukocytes and may be beneficial to develop interventions targeting chemokine C-C motif chemokine ligand 2 for neuroinflammation after spinal cord injury.
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