ArticleJournal of neuroscience research2014
Neuronal and nonneuronal COX-2 expression confers neurotoxic and neuroprotective phenotypes in response to excitotoxin challenge.
Article in Journal of neuroscience research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- PET measurement of cyclooxygenase-2 using a novel radioligand: upregulation in primate neuroinflammation and first-in-human study.Journal of neuroinflammation · 2020Trial
- Blast Overpressure-Induced Neuroinflammation and Axonal Injury in the Spinal Cord of Ferrets.Brain sciences · 2025Article
- Is cyclooxygenase-1 involved in neuroinflammation?Journal of neuroscience research · 2021Review
- Specificity Protein 1: A Protein With a Two-Sided Role in Ischemic Stroke.Frontiers in cellular neuroscience · 2021Review
- Modulation of Neural Networks by Interleukin-1.Brain plasticity (Amsterdam, Netherlands) · 2021Review
- Cyclooxygenase-2 (COX-2) inhibitors: future therapeutic strategies for epilepsy management.Journal of neuroinflammation · 2019Review
- Cell-Type-Specific Interleukin 1 Receptor 1 Signaling in the Brain Regulates Distinct Neuroimmune Activities.Immunity · 2019Article
- Reconceptualization of translocator protein as a biomarker of neuroinflammation in psychiatry.Molecular psychiatry · 2018Review
- Immediate and delayed potentiating effects of tumor necrosis factor-α on TRPV1 sensitivity of rat vagal pulmonary sensory neurons.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Endothelin-1 Induces Degeneration of Cultured Motor Neurons Through a Mechanism Mediated by Nitric Oxide and PI3K/Akt Pathway.Neurotoxicity research · 2017Article
- Inflammation-induced anorexia and fever are elicited by distinct prostaglandin dependent mechanisms, whereas conditioned taste aversion is prostaglandin independent.Brain, behavior, and immunity · 2017Article
- Prostacyclin mediates endothelial COX-2-dependent neuroprotective effects during excitotoxic brain injury.Journal of inflammation research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Treating acute brain injuries with COX-2 inhibitors can produce both neuroprotective and neurotoxic effects. This study investigated the role of COX-2 in modulating acute brain injury induced by excitotoxic neural damage. Intrastriatal injection of excitotoxin (RS)-(tetrazole-5yl) glycine elicited COX-2 expression in two distinct groups of cells. cortical neurons surrounding the lesion and vascular cells in the lesion core. The vascular COX-2 was expressed in two cell types, endothelial cells and monocytes. Selective deletion of COX-2 in vascular cells in Tie2Cre Cox-2(flox/flox) mice did not affect the induction of COX-2 in neurons after the excitotoxin injection but resulted in increased lesion volume, indicating a neuroprotective role for the COX-2 expressed in the vascular cells. Selective deletion of monocyte COX-2 in LysMCre Cox-2(flox/flox) mice did not reduce COX-2-dependent neuroprotection, suggesting that endothelial COX-2 is sufficient to confer neuroprotection. Pharmacological inhibition of COX-2 activity in Tie2Cre Cox-2(flox/flox) mice reduced lesion volume, indicating a neurotoxic role for the COX-2 expressed in neurons. Furthermore, COX-2-dependent neurotoxicity was mediated, at least in part, via the activation of the EP1 receptor. These results show that Cox-2 expression induced in different cell types can confer opposite effects.
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