ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Elevated MMP-9 in the lumbar cord early after thoracic spinal cord injury impedes motor relearning in mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- The effect of early mobilisation (< 14 days) on pathophysiological and functional outcomes in animals with induced spinal cord injury: a systematic review with meta-analysis.BMC neuroscience · 2024Pooled it
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- Biomaterial-Based Emergency Intervention for Secondary Spinal Cord Injury.Small science · 2025Review
- Clickable Granular Hydrogel Scaffolds for Delivery of Neural Progenitor Cells to Sites of Spinal Cord Injury.Advanced healthcare materials · 2024Article
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- Modulating neuroinflammation through molecular, cellular and biomaterial-based approaches to treat spinal cord injury.Bioengineering & translational medicine · 2023Review
- The mechanism of human neural stem cell secretomes improves neuropathic pain and locomotor function in spinal cord injury rat models: through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.The Korean journal of pain · 2023Article
- Effect of Acute Physical Interventions on Pathophysiology and Recovery After Spinal Cord Injury: A Comprehensive Review of the Literature.Neurospine · 2022Article
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- Microglia subtypes show substrate- and time-dependent phagocytosis preferences and phenotype plasticity.Frontiers in immunology · 2022Article
- Meeting Proceedings for SCI 2020: Launching a Decade of Disruption in Spinal Cord Injury Research.Journal of neurotrauma · 2021Review
- Novel approach to an early assessment of a patient's potential for neurological remission after acute spinal cord injury: Analysis of hemoglobin concentration dynamics.The journal of spinal cord medicine · 2021Observational
- Systemic inflammation suppresses spinal respiratory motor plasticity via mechanisms that require serine/threonine protein phosphatase activity.Journal of neuroinflammation · 2021Article
- The neuroanatomical-functional paradox in spinal cord injury.Nature reviews. Neurology · 2021Review
- Behavioral testing in animal models of spinal cord injury.Experimental neurology · 2020Review
- Protein Degradome of Spinal Cord Injury: Biomarkers and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Neuroimmune System as a Driving Force for Plasticity Following CNS Injury.Frontiers in cellular neuroscience · 2020Review
- Spinal cord motor neuron plasticity accompanies second-degree burn injury and chronic pain.Physiological reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal cord injury results in distant pathology around putative locomotor networks that may jeopardize the recovery of locomotion. We previously showed that activated microglia and increased cytokine expression extend at least 10 segments below the injury to influence sensory function. Matrix metalloproteinase-9 (MMP-9) is a potent regulator of acute neuroinflammation. Whether MMP-9 is produced remote to the injury or influences locomotor plasticity remains unexamined. Therefore, we characterized the lumbar enlargement after a T9 spinal cord injury in C57BL/6 (wild-type [WT]) and MMP-9-null (knock-out [KO]) mice. Within 24 h, resident microglia displayed an activated phenotype alongside increased expression of progelatinase MMP-3 in WT mice. By 7 d, increases in active MMP-9 around lumbar vasculature and production of proinflammatory TNF-α were evident. Deletion of MMP-9 attenuated remote microglial activation and restored TNF-α expression to homeostatic levels. To determine whether MMP-9 impedes locomotor plasticity, we delivered lumbar-focused treadmill training in WT and KO mice during early (2-9 d) or late (35-42 d) phases of recovery. Robust behavioral improvements were observed by 7 d, when only trained KO mice stepped in the open field. Locomotor improvements were retained for 4 weeks as identified using state of the art mouse kinematics. Neither training nor MMP-9 depletion alone promoted recovery. The same intervention delivered late was ineffective, suggesting that lesion site sparing is insufficient to facilitate activity-based training and recovery. Our work suggests that by attenuating remote mechanisms of inflammation, acute treadmill training can harness endogenous spinal plasticity to promote robust recovery.
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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.