ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Glucocorticoid receptor-mediated suppression of activator protein-1 activation and matrix metalloproteinase expression after spinal cord injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 115 citations in OpenAlex.
- Matrix Metalloproteinase-9 (MMP-9) as a Therapeutic Target: Insights into Molecular Pathways and Clinical Applications.Pharmaceutics · 2025Review
- Blood-Brain Barrier Disruption in Neuroimmunological Disease.International journal of molecular sciences · 2024Review
- Reviving the use of inhibitors of matrix metalloproteases in spinal cord injury: a case for specificity.Neural regeneration research · 2023Article
- Title: Immunotherapy; a ground-breaking remedy for spinal cord injury with stumbling blocks: An overview.Frontiers in pharmacology · 2023Review
- A Narrative Review on Axonal Neuroprotection in Multiple Sclerosis.Neurology and therapy · 2022Review
- Novel Therapeutic Effects in Rat Spinal Cord Injuries: Recovery of the Definitive and Early Spinal Cord Injury by the Administration of Pentadecapeptide BPC 157 Therapy.Current issues in molecular biology · 2022Article
- The role of EPThe British journal of ophthalmology · 2021Article
- Neutrophil, Extracellular Matrix Components, and Their Interlinked Action in Promoting Secondary Pathogenesis After Spinal Cord Injury.Molecular neurobiology · 2021Review
- Reviewing the Significance of Blood-Brain Barrier Disruption in Multiple Sclerosis Pathology and Treatment.International journal of molecular sciences · 2021Review
- The Endothelial Glycocalyx and Organ Preservation-From Physiology to Possible Clinical Implications for Solid Organ Transplantation.International journal of molecular sciences · 2021Review
- Ursodeoxycholic Acid Inhibits Inflammatory Responses and Promotes Functional Recovery After Spinal Cord Injury in Rats.Molecular neurobiology · 2019Article
- Blood brain barrier (BBB)-disruption in intracortical silicon microelectrode implants.Biomaterials · 2018Article
- Flufenamic acid inhibits secondary hemorrhage and BSCB disruption after spinal cord injury.Theranostics · 2018Article
- Matrix Metalloproteinases During Axonal Regeneration, a Multifactorial Role from Start to Finish.Molecular neurobiology · 2017Review
- Neuroprotective Effects of Direct Intrathecal Administration of Granulocyte Colony-Stimulating Factor in Rats with Spinal Cord Injury.CNS neuroscience & therapeutics · 2015Article
- Dexamethasone Suppressed LPS-Induced Matrix Metalloproteinase and Its Effect on Endothelial Glycocalyx Shedding.Mediators of inflammation · 2015Article
- Dexamethasone ameliorates H₂S-induced acute lung injury by alleviating matrix metalloproteinase-2 and -9 expression.PloS one · 2014Article
- Article
- Neuroprotection and its molecular mechanism following spinal cord injury.Neural regeneration research · 2012Review
- Cannabidiol-treated rats exhibited higher motor score after cryogenic spinal cord injury.Neurotoxicity research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Post-traumatic inflammatory reaction may contribute to progressive tissue damage after spinal cord injury (SCI). Two key transcription factors, nuclear factor kappaB (NF-kappaB) and activator protein-1 (AP-1), are activated in inflammation. An increase in NF-kappaB binding activity has been shown in the injured spinal cord. We report activation of AP-1 after SCI. Electrophoretic mobility shift assay showed that AP-1 binding activity increased after SCI, starting at 1 hr, peaking at 8 hr, and declining to basal levels by 7 d. Methylprednisolone (MP) is the only therapeutic agent approved by the Food and Drug Administration for treating patients with acute traumatic SCI. MP reduced post-traumatic AP-1 activation. RU486, a glucocorticoid receptor (GR) antagonist, reversed MP inhibition of AP-1 activation. Immunostaining showed an increase in the expression of the Fos-B and c-Jun components of AP-1 in the injured cord. A c-fos antisense oligodeoxynucleotide (ODN) inhibited AP-1, but not NF-kappaB, activation after SCI. AP-1 and NF-kappaB can transactivate genes encoding matrix metalloproteinase-1 (MMP-1) and MMP-9. Western blotting and immunostaining show increased expression of MMP-1 and MMP-9 in the injured cord. MP inhibited MMP-1 and MMP-9 expression after SCI. RU486 reversed this MP effect. The c-fos antisense ODN, however, failed to suppress MMP-1 or MMP-9 expression. These findings demonstrate that MP may suppress post-traumatic inflammatory reaction by inhibiting both the AP-1 and NF-kappaB transcription cascades via a GR mechanism. Expression of inflammatory genes such as MMP-1 and MMP-9 that are transactivated jointly by AP-1 and NF-kappaB may not be suppressed by inhibiting only AP-1 activity.
Indexed as
Identifiers
11150324PMC6762457W2102677257What OpenQuestion holds
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.