ArticleJournal of neuroinflammation2014
Deficiency of complement receptors CR2/CR1 in Cr2⁻/⁻ mice reduces the extent of secondary brain damage after closed head injury.
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 18 papers.
What it found
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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.
The trial behind it
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- High plasma complement C4 levels as a novel predictor of clinical outcome in intracerebral hemorrhage.Frontiers in aging neuroscience · 2023Article
- Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Collagen/heparan sulfate porous scaffolds loaded with neural stem cells improve neurological function in a rat model of traumatic brain injury.Neural regeneration research · 2021Article
- Complement mediates neuroinflammation and cognitive decline at extended chronic time points after traumatic brain injury.Acta neuropathologica communications · 2021Article
- Microglia Receptors in Animal Models of Traumatic Brain Injury.Molecular neurobiology · 2019Review
- Significance of Complement System in Ischemic Stroke: A Comprehensive Review.Aging and disease · 2019Review
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System.Frontiers in immunology · 2019Review
- Relationship of calcitonin gene-related peptide with disease progression and prognosis of patients with severe traumatic brain injury.Neural regeneration research · 2018Article
- Complement After Trauma: Suturing Innate and Adaptive Immunity.Frontiers in immunology · 2018Review
- C5a/C5aR Pathway Plays a Vital Role in Brain Inflammatory Injury via Initiating Fgl-2 in Intracerebral Hemorrhage.Molecular neurobiology · 2017Article
- α7 nicotinic acetylcholine receptor signaling modulates the inflammatory phenotype of fetal brain microglia: first evidence of interference by iron homeostasis.Scientific reports · 2017Article
- Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice.Science translational medicine · 2017Article
- IVIg attenuates complement and improves spinal cord injury outcomes in mice.Annals of clinical and translational neurology · 2016Article
- Complement receptor 2 is up regulated in the spinal cord following nerve root injury and modulates the spinal cord response.Journal of neuroinflammation · 2015Article
- Current and future implications of basic and translational research on amyloid-β peptide production and removal pathways.Molecular and cellular neurosciences · 2015Review
- A new mouse anti-mouse complement receptor type 2 and 1 (CR2/CR1) monoclonal antibody as a tool to study receptor involvement in chronic models of immune responses and disease.Molecular immunology · 2015Article
- Complement, thrombotic microangiopathy and disseminated intravascular coagulation.Journal of intensive care · 2014Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Complement activation at the C3 convertase level has been associated with acute neuroinflammation and secondary brain injury after severe head trauma. The present study was designed to test the hypothesis that Cr2-/- mice, which lack the receptors CR2/CD21 and CR1/CD35 for complement C3-derived activation fragments, are protected from adverse sequelae of experimental closed head injury. Adult wild-type mice and Cr2-/- mice on a C57BL/6 genetic background were subjected to focal closed head injury using a standardized weight-drop device. Head-injured Cr2-/- mice showed significantly improved neurological outcomes for up to 72 hours after trauma and a significantly decreased post-injury mortality when compared to wild-type mice. In addition, the Cr2-/- genotype was associated with a decreased extent of neuronal cell death at seven days post-injury. Western blot analysis revealed that complement C3 levels were reduced in the injured brain hemispheres of Cr2-/- mice, whereas plasma C3 levels remained unchanged, compared to wild-type mice. Finally, head-injured Cr2-/- had an attenuated extent of post-injury C3 tissue deposition, decreased astrocytosis and microglial activation, and attenuated immunoglobulin M deposition in injured brains compared to wild-type mice. Targeting of these receptors for complement C3 fragments (CR2/CR1) may represent a promising future approach for therapeutic immunomodulation after traumatic brain injury.
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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.