ArticleBMC neuroscience2016
Glutamate carboxypeptidase II gene knockout attenuates oxidative stress and cortical apoptosis after traumatic brain injury.
Article in BMC neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Fer-1 alleviates traumatic brain injury-induced cognitive impairment by inhibiting hippocampal ferroptosis.IBRO neuroscience reports · 2025Article
- Deletion of glutamate carboxypeptidase II (GCPII), but not GCPIII, provided long-term benefits in mice with traumatic brain injury.CNS neuroscience & therapeutics · 2023Article
- Scientific rationale for the use of α2A-adrenoceptor agonists in treating neuroinflammatory cognitive disorders.Molecular psychiatry · 2023Review
- Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis.CNS neuroscience & therapeutics · 2023Review
- A gut-restricted glutamate carboxypeptidase II inhibitor reduces monocytic inflammation and improves preclinical colitis.Science translational medicine · 2023Article
- Novel neuroendocrine role of γ-aminobutyric acid and gastrin-releasing peptide in the host response to influenza infection.Mucosal immunology · 2023Article
- Article
- ILBInternational journal of molecular sciences · 2022Article
- The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia.Cell communication and signaling : CCS · 2022Article
- Review
- Review
- Glutamate Carboxypeptidase II in Aging Rat Prefrontal Cortex Impairs Working Memory Performance.Frontiers in aging neuroscience · 2021Article
- Pretreatment with mGluR2 or mGluR3 Agonists Reduces Apoptosis Induced by Hypoxia-Ischemia in Neonatal Rat Brains.Oxidative medicine and cellular longevity · 2021Article
- The Emerging Role of Sestrin2 in Cell Metabolism, and Cardiovascular and Age-Related Diseases.Aging and disease · 2020Review
- Polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria.Neural regeneration research · 2019Article
- UPLC-QTOF/MS-Based Metabolomics Reveals the Protective Mechanism of Hydrogen on Mice with Ischemic Stroke.Neurochemical research · 2019Article
- Acute histopathological responses and long-term behavioral outcomes in mice with graded controlled cortical impact injury.Neural regeneration research · 2019Article
- Inhibition of ferroptosis attenuates tissue damage and improves long-term outcomes after traumatic brain injury in mice.CNS neuroscience & therapeutics · 2019Article
- Metabolite differences between glutamate carboxypeptidase II gene knockout mice and their wild-type littermates after traumatic brain injury: a 7-teslaBMC neuroscience · 2018Article
- Inhibition of endoplasmic reticulum stress alleviates secondary injury after traumatic brain injury.Neural regeneration research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlutamate carboxypeptidase II (GCPII) inactivates the peptide co-transmitter N-acetylaspartylglutamate following synaptic release. Inhibition of GCPII elevates extracellular levels of the peptide, inhibits glutamate release and is neuroprotective in an animal model of traumatic brain injury. GCPII gene knockout mice were used to examine the cellular mechanisms underlying the neuroprotective efficacy of this transmitter system.
resultsFollowing controlled cortical impact injury, GCPII knockout (KO) mice exhibited reduced TUNEL-positive nuclei in the contusion margin of the cerebral cortex relative to wild type mice. Impact injury reduced glutathione levels and superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde. Each of these effects was moderated in KO mice relative to wild type. Similarly, the injury-induced increases in cleaved caspase-3, cytosolic cytochrome c levels and Bcl-2/Bax ratio observed in wild type mice were attenuated in the knockout mice.
conclusionsThese data support the hypothesis that the neuroprotective efficacy of GCPII KO in traumatic brain injury is mediated via a reduction in oxidative stress.
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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.