ArticleJournal of neuroinflammation2018
Macrophage migration inhibitory factor facilitates production of CCL5 in astrocytes following rat spinal cord injury.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Immunoregulation of Glia after spinal cord injury: a bibliometric analysis.Frontiers in immunology · 2024Pooled it
- Macrophage migration inhibitory factor as a therapeutic target after traumatic spinal cord injury: a systematic review.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2021Pooled it
- Neuroprotection and immunomodulation after treatment with NeuroBoost and NeuroHeal following ventral root crush in mice.IBRO neuroscience reports · 2026Article
- Enhanced MIF/CD74 axis activity shapes B cell functioning following traumatic spinal cord injury.Journal of neuroinflammation · 2026Article
- Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- 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
- MIF Inhibition by ISO-1 Decreased Autophagic Activity in Primary Astrocytes During Cobalt Chloride-Induced Hypoxia.Current issues in molecular biology · 2024Article
- Macrophage migration inhibitory factor (MIF) in CNS diseases: Functional regulation and potential therapeutic indication.Fundamental research · 2024Review
- Article
- Osteoimmune Interaction and TH-1/TH-2 Ratio in Jawbone Marrow Defects: An Underestimated Association - Original Research.Biologics : targets & therapy · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- HIF-1α promotes astrocytic production of macrophage migration inhibitory factor following spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- Macrophage migration inhibitory factor facilitates astrocytic production of the CCL2 chemokine following spinal cord injury.Neural regeneration research · 2023Article
- The Role of Mesenchymal Stromal Cells and Their Products in the Treatment of Injured Spinal Cords.Current issues in molecular biology · 2023Review
- Thrombin increases the expression of cholesterol 25-hydroxylase in rat astrocytes after spinal cord injury.Neural regeneration research · 2023Article
- Current Advancements in Spinal Cord Injury Research-Glial Scar Formation and Neural Regeneration.Cells · 2023Review
- D-dopachrome tautomerase drives astroglial inflammation via NF-κB signaling following spinal cord injury.Cell & bioscience · 2022Article
- Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury.Journal of neuroinflammation · 2022Article
- Thrombin induces morphological and inflammatory astrocytic responses via activation of PAR1 receptor.Cell death discovery · 2022Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAstrocytes act as immune effector cells with the ability to produce a wide array of chemokines and cytokines in response to various stimuli. Macrophage migration inhibitory factor (MIF) is inducibly expressed in injured spinal cord contributing to excessive inflammation that affects motor functional recovery. Unknown is whether MIF can facilitate inflammatory responses through stimulating release of chemokines from astrocytes following spinal cord injury.
methodsFollowing the establishment of the contusion spinal cord injury rat model, the correlation of chemokine (C-C motif) ligand 5 (CCL5) expression with that of MIF was assayed by Western blot, ELISA, and immunohistochemistry. Immunoprecipitation was used to detect MIF interaction with membrane CD74 receptor. Intracellular signal transduction of MIF/CD74 axis was analyzed by transcriptome sequencing of primary astrocytes and further validated by treatment of various inhibitors. The effects of CCL5 released by astrocytes on macrophage migration were performed by transwell migration assay. The post-injury locomotor functions were assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor scale.
resultsThe protein levels of chemokine CCL5/RANTES were remarkably increased in the astrocytes of rat injured spinal cord, in parallel with the expression of MIF. Treatment of MIF inhibitor 4-IPP in the lesion sites resulted in a significant decrease of CCL5 protein levels. In vitro study revealed MIF was capable of facilitating CCL5 production of astrocytes through interaction with CD74 membrane receptor, and knockdown of this receptor attenuated such effects. Production of CCL5 in astrocytes was significantly blocked by inhibitor of c-Jun N-terminal kinase, rather than by those of ERK and P38. Recombinant CCL5 protein was found to be more effective in promoting migration of M2- compared to M1-type macrophages.
conclusionCollectively, these data reveal a novel function of MIF in regulation of CCL5 release from astrocytes, which in turn favors for recruitment of inflammatory cells to the injured site of the spinal cord, in association with activation of excessive inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.