ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Overcoming macrophage-mediated axonal dieback following CNS injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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Who cites it
130 citing papers in PubMed, 217 citations in OpenAlex.
- Role of Pattern Recognition Receptors (PRRs) in Spinal Cord Injury (SCI): A Comprehensive Review.Molecular neurobiology · 2026Review
- Notch Signaling in Spinal Cord Injury: Mechanistic Insights and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- An integrated analysis of spinal cord transcriptome and gut microbiome unravel age-associated host-microbiome interactions following spinal cord injury.Frontiers in immunology · 2026Article
- Remote neurodegeneration in the lumbosacral cord one month after spinal cord injury: a cross-sectional MRI study.Annals of clinical and translational neurology · 2025Article
- Nonresolving Neuroinflammation Regulates Axon Regeneration in Chronic Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- RNA Interference Unleashed: Current Perspective of Small Interfering RNA (siRNA) Therapeutics in the Treatment of Neuropathic Pain.ACS pharmacology & translational science · 2024Review
- High mobility group box-1 protein promotes astrocytic CCL5 production through the MAPK/NF-κB pathway following spinal cord injury.Scientific reports · 2024Article
- Opportunities and challenges in design and optimization of protein function.Nature reviews. Molecular cell biology · 2024Review
- Neither injury induced macrophages within the nerve, nor the environment created by Wallerian degeneration is necessary for enhanced in vivo axon regeneration after peripheral nerve injury.Journal of neuroinflammation · 2024Article
- Non-resolving neuroinflammation regulates axon regeneration in chronic spinal cord injury.bioRxiv : the preprint server for biology · 2024Article
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- Reviving the use of inhibitors of matrix metalloproteases in spinal cord injury: a case for specificity.Neural regeneration research · 2023Article
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- Unleashing Spinal Cord Repair: The Role of cAMP-Specific PDE Inhibition in Attenuating Neuroinflammation and Boosting Regeneration after Traumatic Spinal Cord Injury.International journal of molecular sciences · 2023Review
- Tackling the glial scar in spinal cord regeneration: new discoveries and future directions.Frontiers in cellular neuroscience · 2023Review
- Pathophysiology and Therapeutic Approaches for Spinal Cord Injury.International journal of molecular sciences · 2022Review
- Ruxolitinib attenuates secondary injury after traumatic spinal cord injury.Neural regeneration research · 2022Article
- Long-term in vivo imaging of mouse spinal cord through an optically cleared intervertebral window.Nature communications · 2022Article
- New insights into glial scar formation after spinal cord injury.Cell and tissue research · 2022Review
- Intestinal microbiota and melatonin in the treatment of secondary injury and complications after spinal cord injury.Frontiers in neuroscience · 2022Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Trauma to the adult CNS initiates multiple processes including primary and secondary axotomy, inflammation, and glial scar formation that have devastating effects on neuronal regeneration. After spinal cord injury, the infiltration of phagocytic macrophages coincides with long-distance axonal retraction from the initial site of injury, a deleterious phenomenon known as axonal dieback. We have previously shown that activated macrophages directly induce long-distance retraction of dystrophic axons in an in vitro model of the glial scar. We hypothesized that treatments that are primarily thought to increase neuronal regeneration following spinal cord injury may in fact derive a portion of their beneficial effects from inhibition of macrophage-mediated axonal retraction. We analyzed the effects of protease inhibition, substrate modification, and neuronal preconditioning on macrophage-axon interactions using our established in vitro model. General inhibition of matrix metalloproteinases and specific inhibition of MMP-9 prevented macrophage-induced axonal retraction despite significant physical interactions between the two cell types, whereas inhibition of MMP-2 had no effect. Chondroitinase ABC-mediated digestion of the aggrecan substrate also prevented macrophage-induced axonal retraction in the presence of extensive macrophage-axon interactions. The use of a conditioning lesion to stimulate intrinsic neuronal growth potential in the absence of substrate modification likewise prevented macrophage-induced axonal retraction in vitro and in vivo following spinal cord injury. These data provide valuable insight into the cellular and molecular mechanisms underlying macrophage-mediated axonal retraction and demonstrate modifications that can alleviate the detrimental effects of this unfavorable phenomenon on the postlesion CNS.
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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.