ArticleBrain, behavior, and immunity2017
Reciprocal relationship between membrane type 1 matrix metalloproteinase and the algesic peptides of myelin basic protein contributes to chronic neuropathic pain.
Article in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Trial
- The Hypothesis of Myelinodegeneration as an Initial Risk of Neuropathic Pain.Neuroscience bulletin · 2026Review
- Pain kept under wraps of myelin sheath.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Cholesterol-dependent LXR transcription factor activity represses pronociceptive effects of estrogen in sensory neurons and pain induced by myelin basic protein fragments.Brain, behavior, & immunity - health · 2024Article
- Comparison of N-Glycopeptide to Released N-Glycan Abundances and the Influence of Glycopeptide Mass and Charge States on N-Linked Glycosylation of IgG Antibodies.Journal of proteome research · 2024Article
- SPOCK2 modulates neuropathic pain by interacting with MT1-MMP to regulate astrocytic MMP-2 activation in rats with chronic constriction injury.Journal of neuroinflammation · 2024Article
- The Effect of Differentiation of Human Dental Pulp Stem Cells to Glial Cells on the Sensory Nerves of the Dental Pulp.International journal of dentistry · 2024Article
- UNC5B Overexpression Alleviates Peripheral Neuropathic Pain by Stimulating Netrin-1-Dependent Autophagic Flux in Schwann Cells.Molecular neurobiology · 2022Article
- A human coronavirus OC43-derived polypeptide causes neuropathic pain.EMBO reports · 2022Article
- Sex-Specific B Cell and Anti-Myelin Autoantibody Response After Peripheral Nerve Injury.Frontiers in cellular neuroscience · 2022Article
- Mammalian Sterile 20-Like Kinase 1 Mediates Neuropathic Pain Associated with Its Effects on Regulating Mitophagy in Schwann Cells.Oxidative medicine and cellular longevity · 2022Article
- A myelin basic protein fragment induces sexually dimorphic transcriptome signatures of neuropathic pain in mice.The Journal of biological chemistry · 2020Article
- Emerging Role of Schwann Cells in Neuropathic Pain: Receptors, Glial Mediators and Myelination.Frontiers in cellular neuroscience · 2019Review
- Tissue inhibitors of metalloproteases strike a nerve.Neural regeneration research · 2018Article
- Amino acid sequence conservation of the algesic fragment of myelin basic protein is required for its interaction with CDK5 and function in pain.The FEBS journal · 2018Article
- Interaction of the cryptic fragment of myelin basic protein with mitochondrial voltage-dependent anion-selective channel-1 affects cell energy metabolism.The Biochemical journal · 2018Article
- A sensitive and selective ELISA methodology quantifies a demyelination marker in experimental and clinical samples.Journal of immunological methods · 2018Article
- Acute- and late-phase matrix metalloproteinase (MMP)-9 activity is comparable in female and male rats after peripheral nerve injury.Journal of neuroinflammation · 2018Article
- Matrix metalloproteinases - From the cleavage data to the prediction tools and beyond.Biochimica et biophysica acta. Molecular cell research · 2017Review
- Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Myelin basic protein (MBP) is an auto-antigen able to induce intractable pain from innocuous mechanical stimulation (mechanical allodynia). The mechanisms provoking this algesic MBP activity remain obscure. Our present study demonstrates that membrane type 1 matrix metalloproteinase (MT1-MMP/MMP-14) releases the algesic MBP peptides from the damaged myelin, which then reciprocally enhance the expression of MT1-MMP in nerve to sustain a state of allodynia. Specifically, MT1-MMP expression and activity in rat sciatic nerve gradually increased starting at day 3 after chronic constriction injury (CCI). Inhibition of the MT1-MMP activity by intraneural injection of the function-blocking human DX2400 monoclonal antibody at day 3 post-CCI reduced mechanical allodynia and neuropathological signs of Wallerian degeneration, including axon demyelination, degeneration, edema and formation of myelin ovoids. Consistent with its role in allodynia, the MT1-MMP proteolysis of MBP generated the MBP69-86-containing epitope sequences in vitro. In agreement, the DX2400 therapy reduced the release of the MBP69-86 epitope in CCI nerve. Finally, intraneural injection of the algesic MBP69-86 and control MBP2-18 peptides differentially induced MT1-MMP and MMP-2 expression in the nerve. With these data we offer a novel, self-sustaining mechanism of persistent allodynia via the positive feedback loop between MT1-MMP and the algesic MBP peptides. Accordingly, short-term inhibition of MT1-MMP activity presents a feasible pharmacological approach to intervene in this molecular circuit and the development of neuropathic pain.
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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.