ArticleCNS neuroscience & therapeutics2023
HIF-1α promotes astrocytic production of macrophage migration inhibitory factor following spinal cord injury.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- MIF Tautomerase Inhibition Protects Neurons From Immune-Mediated Cell Death.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Enhanced MIF/CD74 axis activity shapes B cell functioning following traumatic spinal cord injury.Journal of neuroinflammation · 2026Article
- Obacunone Promotes Functional Recovery After Spinal Cord Injury by Attenuating Neuroinflammation by Targeting the TLR4/MyD88/p38 MAPK Pathway.Drug design, development and therapy · 2026Article
- Regulation of dynamic spatiotemporal inflammation by nanomaterials in spinal cord injury.Journal of nanobiotechnology · 2024Review
- MIF Inhibition by ISO-1 Decreased Autophagic Activity in Primary Astrocytes During Cobalt Chloride-Induced Hypoxia.Current issues in molecular biology · 2024Article
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- HIF-1α promotes astrocytic production of macrophage migration inhibitory factor following spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- Highly Selective MIF Ketonase Inhibitor KRP-6 Diminishes M1 Macrophage Polarization and Metabolic Reprogramming.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMacrophage migration inhibitory factor (MIF) is an important mediator of neuropathology in various central nervous system (CNS) diseases. However, little is known about its inducers for production from the nerve cells, as well as the underlying regulatory mechanism. Injury-induced HIF-1α has been shown to exacerbate neuroinflammation by activating multiple downstream target molecules. It is postulated that HIF-1α is involved in the regulation of MIF following spinal cord injury (SCI).
methodsSCI model of Sprague-Dawley rats was established by cord contusion at T8-T10. The dynamic changes of HIF-1α and MIF protein levels at lesion site of rat spinal cord were determined by Western blot. The specific cell types of HIF-1α and MIF expression were examined by immunostaining. Primary astrocytes were isolated from the spinal cord, cultured and stimulated with various agonist or inhibitor of HIF-1α for analysis of HIF-1α-mediated expression of MIF. Luciferase report assay was used to determine the relationship between HIF-1α and MIF. The Basso, Beattie, and Bresnahan (BBB) locomotor scale was used to assess the locomotor function following SCI.
resultsThe protein levels of HIF-1α and MIF at lesion site were significantly elevated by SCI. Immunofluorescence demonstrated that both HIF-1α and MIF were abundantly expressed in the astrocytes of the spinal cord. By using various agonists or inhibitors of HIF-1α, it was shown that HIF-1α sufficiently induced astrocytic production of MIF. Mechanistically, HIF-1α promoted MIF expression through interaction with MIF promoter. Inhibition of HIF-1α activity using specific inhibitor markedly reduced the protein levels of MIF at lesion site following SCI, which in turn favored for the functional recovery.
conclusionSCI-induced activation of HIF-1α is able to promote MIF production from astrocytes. Our results have provided new clues for SCI-induced production of DAMPs, which may be helpful for clinical treatment of neuroinflammation.
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