ArticleThe American journal of pathology2010
MCP-1/CCL2 modifies axon properties in a PMP22-overexpressing mouse model for Charcot-Marie-tooth 1A neuropathy.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 60 citations in OpenAlex.
- Reactive aldehyde species-mediated neuropathic pain in spinal cord injury: Mechanisms and therapeutic opportunities.Neural regeneration research · 2026Article
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Biomarkers and Novel Therapies of Diabetic Neuropathy: An Updated Review.Current pharmaceutical biotechnology · 2025Review
- Mechanisms and treatment strategies of demyelinating and dysmyelinating Charcot-Marie-Tooth disease.Neural regeneration research · 2023Review
- Pharmacologic Targeting of the C-Terminus of Heat Shock Protein 90 Improves Neuromuscular Function in Animal Models of Charcot Marie Tooth X1 Disease.ACS pharmacology & translational science · 2023Article
- NCAM1 and GDF15 are biomarkers of Charcot-Marie-Tooth disease in patients and mice.Brain : a journal of neurology · 2022Article
- HDAC3 Inhibition Stimulates Myelination in a CMT1A Mouse Model.Molecular neurobiology · 2022Article
- The macrophage: a key player in the pathophysiology of peripheral neuropathies.Journal of neuroinflammation · 2022Review
- Inflammatory Mechanisms in the Pathophysiology of Diabetic Peripheral Neuropathy (DN)-New Aspects.International journal of molecular sciences · 2021Review
- New evidence for secondary axonal degeneration in demyelinating neuropathies.Neuroscience letters · 2021Review
- Intra-axonal mechanisms driving axon regeneration.Brain research · 2020Review
- AfterNeuro-oncology advances · 2020Review
- Comparison of three congruent patient-specific cell types for the modelling of a human genetic Schwann-cell disorder.Nature biomedical engineering · 2019Article
- NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies.Nature communications · 2019Article
- Fingolimod phosphate inhibits astrocyte inflammatory activity in mucolipidosis IV.Human molecular genetics · 2018Article
- Deletion of MCP-1 Impedes Pathogenesis of Acid Ceramidase Deficiency.Scientific reports · 2018Article
- Sustained MAPK/ERK Activation in Adult Schwann Cells Impairs Nerve Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Dysregulation of ErbB Receptor Trafficking and Signaling in Demyelinating Charcot-Marie-Tooth Disease.Molecular neurobiology · 2017Review
- The crucial role of Erk2 in demyelinating inflammation in the central nervous system.Journal of neuroinflammation · 2016Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Charcot-Marie-Tooth 1A (CMT1A) neuropathy, the most common inherited peripheral neuropathy, is primarily caused by a gene duplication for the peripheral myelin protein-22 (PMP22). In an accordant mouse model, we investigated the role of monocyte chemoattractant protein-1 (MCP-1/CCL2) as a regulator of nerve macrophages and neural damage including axonopathy and demyelination. By generating PMP22tg mice with reduced levels or lack of MCP-1/CCL2, we found that MCP-1/CCL2 is involved in the increase of macrophages in mutant nerves. PMP22tg mice with wild-type levels of MCP-1/CCL2 showed strong macrophage increase in the diseased nerves, whereas either 50% reduction or total absence of MCP-1/CCL2 led to a moderate or a strong reduction of nerve macrophages, respectively. Interestingly, MCP-1/CCL2 expression level and macrophage numbers were correlated with features indicative of axon damage, such as maldistribution of K+ channels, reduced compound muscle action potentials, and muscle weakness. Demyelinating features, however, were most highly reduced when MCP-1/CCL2 was diminished by 50%, whereas complete lack of MCP-1/CCL2 showed an intermediate demyelinating phenotype. We also identified the MEK1/2-ERK1/2-pathway as being involved in MCP-1/CCL2 expression in the Schwann cells of the CMT1A model. Our data show that, in a CMT1A model, MCP-1/CCL2 activates nerve macrophages, mediates both axon damage and demyelination, and may thus be a promising target for therapeutic approaches.
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