ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Deficiency in complement C1q improves histological and functional locomotor outcome after spinal cord injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Targeting complement and coagulation cascades with Buyang Huanwu Decoction attenuates acute inflammation and enhances neuroprotection in spinal cord injury.Science China. Life sciences · 2026Article
- APOE-mediated lipid transport prevents C1q-related synaptic loss after spinal cord injury via attenuating macrophage lipid stress.Journal of neuroinflammation · 2026Article
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CD44 Knockout Alters the Cellular Response and Improves Locomotor Outcome After Spinal Cord Injury.ASN neuro · 2026Article
- Lipid accumulation in foam cells drives C1q-dependent synaptic loss and impairs motor function recovery after spinal cord injury.Communications biology · 2025Article
- C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.Nature communications · 2025Article
- Immune Activation Following Spinal Cord Injury: A Review Focused on Inflammatory Changes in the Spinal Cord.International journal of molecular sciences · 2025Review
- Complement Factor B Deficiency Is Dispensable for Female Fertility but Affects Microbiome Diversity and Complement Activity.International journal of molecular sciences · 2025Article
- C1q and central nervous system disorders.Frontiers in immunology · 2023Review
- C1q and the classical complement cascade in geographic atrophy secondary to age-related macular degeneration.International journal of retina and vitreous · 2022Review
- Review
- Sexual Dimorphism in Lesion Size and Sensorimotor Responses Following Spinal Cord Injury.Frontiers in neurology · 2022Article
- Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Acute inflammatory profiles differ with sex and age after spinal cord injury.Journal of neuroinflammation · 2021Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Initiators of Classical and Lectin Complement Pathways Are Differently Engaged after Traumatic Brain Injury-Time-Dependent Changes in the Cortex, Striatum, Thalamus and Hippocampus in a Mouse Model.International journal of molecular sciences · 2020Article
- Complement C6 deficiency exacerbates pathophysiology after spinal cord injury.Scientific reports · 2020Article
- Effect of VX‑765 on the transcriptome profile of mice spinal cords with acute injury.Molecular medicine reports · 2020Article
- An "Outside-In" and "Inside-Out" Consideration of Complement in the Multiple Sclerosis Brain: Lessons From Development and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Although studies have suggested a role for the complement system in the pathophysiology of spinal cord injury (SCI), that role remains poorly defined. Additionally, the relative contribution of individual complement pathways in SCI is unknown. Our initial studies revealed that systemic complement activation was strongly influenced by genetic background and gender. Thus, to investigate the role of the classical complement pathway in contusion-induced SCI, male C1q knock-out (KO) and wild-type (WT) mice on a complement sufficient background (BUB) received a mild-moderate T9 contusion injury with the Infinite Horizon impactor. BUB C1q KO mice exhibited greater locomotor recovery compared with BUB WT mice (p<0.05). Improved recovery observed in BUB C1q KO mice was also associated with decreased threshold for withdrawal from a mild stimulus using von Frey filament testing. Surprisingly, quantification of microglia/macrophages (F4/80) by FACS analysis showed that BUB C1q KO mice exhibited a significantly greater percentage of macrophages in the spinal cord compared with BUB WT mice 3 d post-injury (p<0.05). However, this increased macrophage response appeared to be transient as stereological assessment of spinal cord tissue obtained 28 d post-injury revealed no difference in F4/80-positive cells between groups. Stereological assessment of spinal cord tissue showed that BUB C1q KO mice had reduced lesion volume and an increase in tissue sparing compared with BUB WT mice (p<0.05). Together, these data suggest that initiation of the classical complement pathway via C1q is detrimental to recovery after SCI.
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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.