ArticleJournal of neuroinflammation2009
Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice.
Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Molecular characterization ofOpen veterinary journal · 2026Article
- Targeted complement inhibition ameliorates the pathological and cognitive outcomes in repetitive mild closed head injury.Signal transduction and targeted therapy · 2025Article
- Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- 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
- Transcriptome analysis reveals genes associated with stem cell activation by physical exercise in the dentate gyrus of aged p16Ink4a knockout mice.Frontiers in cell and developmental biology · 2023Article
- Age Worsens the Cognitive Phenotype in Mice Carrying the Thr92Ala-DIO2 Polymorphism.Metabolites · 2022Article
- Article
- Soluble terminal complement activation fragment sC5b-9: a new serum biomarker for traumatic brain injury?European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2021Observational
- Ethanol modulation of cerebellar neuroinflammation in a postnatal mouse model of fetal alcohol spectrum disorders.Journal of neuroscience research · 2021Article
- Comparative transcriptomic analysis of ratNeural regeneration research · 2021Article
- Proteomic Profiling of the Substantia Nigra to Identify Determinants of Lewy Body Pathology and Dopaminergic Neuronal Loss.Journal of proteome research · 2021Article
- Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021Review
- Fluid proteomics of CSF and serum reveal important neuroinflammatory proteins in blood-brain barrier disruption and outcome prediction following severe traumatic brain injury: a prospective, observational study.Critical care (London, England) · 2021Observational
- Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The Immune System's Role in the Consequences of Mild Traumatic Brain Injury (Concussion).Frontiers in immunology · 2021Review
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Targeted deletions of complement lectin pathway genes improve outcome in traumatic brain injury, with MASP-2 playing a major role.Acta neuropathologica communications · 2020Article
- Increased Macrophages and C1qA, C3, C4 Transcripts in the Midbrain of People With Schizophrenia.Frontiers in immunology · 2020Article
- Inflammation in Traumatic Brain Injury.Journal of Alzheimer's disease : JAD · 2020Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundComplement represents a crucial mediator of neuroinflammation and neurodegeneration after traumatic brain injury. The role of the terminal complement activation pathway, leading to generation of the membrane attack complex (MAC), has not been thoroughly investigated. CD59 is the major regulator of MAC formation and represents an essential protector from homologous cell injury after complement activation in the injured brain.
methodsMice deleted in the Cd59a gene (CD59a-/-) and wild-type littermates (n = 60) were subjected to focal closed head injury. Sham-operated (n = 60) and normal untreated mice (n = 14) served as negative controls. The posttraumatic neurological impairment was assessed for up to one week after trauma, using a standardized Neurological Severity Score (NSS). The extent of neuronal cell death was determined by serum levels of neuron-specific enolase (NSE) and by staining of brain tissue sections in TUNEL technique. The expression profiles of pro-apoptotic (Fas, FasL, Bax) and anti-apoptotic (Bcl-2) mediators were determined at the gene and protein level by real-time RT-PCR and Western blot, respectively.
resultsClinically, the brain-injured CD59a-/- mice showed a significantly impaired neurological outcome within 7 days, as determined by a higher NSS, compared to wild-type controls. The NSE serum levels, an indirect marker of neuronal cell death, were significantly elevated in CD59a-/- mice at 4 h and 24 h after trauma, compared to wild-type littermates. At the tissue level, increased neuronal cell death and brain tissue destruction was detected by TUNEL histochemistry in CD59a-/- mice within 24 hours to 7 days after head trauma. The analysis of brain homogenates for potential mediators and regulators of cell death other than the complement MAC (Fas, FasL, Bax, Bcl-2) revealed no difference in gene expression and protein levels between CD59a-/- and wild-type mice.
conclusionThese data emphasize an important role of CD59 in mediating protection from secondary neuronal cell death and further underscore the key role of the terminal complement pathway in the pathophysiology of traumatic brain injury. The exact mechanisms of complement MAC-induced secondary neuronal cell death after head injury require further investigation.
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