ArticleJournal of neuroinflammation2014
Inflammatory cascades mediate synapse elimination in spinal cord compression.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The Pathophysiology of Degenerative Cervical Myelopathy and the Physiology of Recovery Following Decompression.Frontiers in neuroscience · 2020Pooled it
- Incidence and costs of cervical spondylosis in urban China from 2013 to 2017: a nationwide population-based study.The Lancet regional health. Western Pacific · 2026Article
- An Examination of the Role of CX3CR1 in the Pathobiology of Degenerative Cervical Myelopathy: Evidence from Human and Mouse Tissue.Journal of clinical medicine · 2025Article
- TLR3 Knockdown Attenuates Pressure-Induced Neuronal Damage In Vitro.Journal of cellular and molecular medicine · 2024Article
- Visual cortical plasticity and the risk for psychosis: An interim analysis of the North American Prodrome Longitudinal Study.Schizophrenia research · 2021Article
- Amyloid Fibril-Induced Astrocytic Glutamate Transporter Disruption Contributes to Complement C1q-Mediated Microglial Pruning of Glutamatergic Synapses.Molecular neurobiology · 2020Article
- MicroRNA-181 regulates the development of Ossification of Posterior longitudinal ligament via Epigenetic Modulation by targeting PBX1.Theranostics · 2020Article
- Transcriptome Analysis Reveals the Effects of Troxerutin and Cerebroprotein Hydrolysate Injection on Injured Spinal Cords in Rats.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.Molecular neurobiology · 2019Article
- Lower level noise exposure that produces only TTS modulates the immune homeostasis of cochlear macrophages.Journal of neuroimmunology · 2018Article
- Correlation between the severity of myelopathy and cervical morphometric parameters on dynamic magnetic resonance imaging.Acta neurochirurgica · 2018Article
- Association between Cervical Spondylosis and Migraine: A Nationwide Retrospective Cohort Study.International journal of environmental research and public health · 2018Article
- Article
- C1 Complex: An Adaptable Proteolytic Module for Complement and Non-Complement Functions.Frontiers in immunology · 2017Review
- Association Between Microglia, Inflammatory Factors, and Complement with Loss of Hippocampal Mossy Fiber Synapses Induced by Trimethyltin.Neurotoxicity research · 2016Article
- The incidence of cervical spondylosis decreases with aging in the elderly, and increases with aging in the young and adult population: a hospital-based clinical analysis.Clinical interventions in aging · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCervical compressive myelopathy (CCM) is caused by chronic spinal cord compression due to spondylosis, a degenerative disc disease, and ossification of the ligaments. Tip-toe walking Yoshimura (twy) mice are reported to be an ideal animal model for CCM-related neuronal dysfunction, because they develop spontaneous spinal cord compression without any artificial manipulation. Previous histological studies showed that neurons are lost due to apoptosis in CCM, but the mechanism underlying this neurodegeneration was not fully elucidated. The purpose of this study was to investigate the pathophysiology of CCM by evaluating the global gene expression of the compressed spinal cord and comparing the transcriptome analysis with the physical and histological findings in twy mice.
methodsTwenty-week-old twy mice were divided into two groups according to the magnetic resonance imaging (MRI) findings: a severe compression (S) group and a mild compression (M) group. The transcriptome was analyzed by microarray and RT-PCR. The cellular pathophysiology was examined by immunohistological analysis and immuno-electron microscopy. Motor function was assessed by Rotarod treadmill latency and stride-length tests.
resultsSevere cervical calcification caused spinal canal stenosis and low functional capacity in twy mice. The microarray analysis revealed 215 genes that showed significantly different expression levels between the S and the M groups. Pathway analysis revealed that genes expressed at higher levels in the S group were enriched for terms related to the regulation of inflammation in the compressed spinal cord. M1 macrophage-dominant inflammation was present in the S group, and cysteine-rich protein 61 (Cyr61), an inducer of M1 macrophages, was markedly upregulated in these spinal cords. Furthermore, C1q, which initiates the classical complement cascade, was more upregulated in the S group than in the M group. The confocal and electron microscopy observations indicated that classically activated microglia/macrophages had migrated to the compressed spinal cord and eliminated synaptic terminals.
conclusionsWe revealed the detailed pathophysiology of the inflammatory response in an animal model of chronic spinal cord compression. Our findings suggest that complement-mediated synapse elimination is a central mechanism underlying the neurodegeneration in CCM.
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