ArticleNeurotoxicity research2009
PGF(2alpha) FP receptor contributes to brain damage following transient focal brain ischemia.
Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- Ischemic Brain Injury: Involvement of Lipids in the Pathophysiology of Stroke and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2024Review
- Associations between oxidative stress biomarkers during pregnancy and infant cognition at 7.5 months.Developmental psychobiology · 2024Article
- Neuroaxonal and cellular damage/protection by prostanoid receptor ligands, fatty acid derivatives and associated enzyme inhibitors.Neural regeneration research · 2023Review
- G-Protein-Coupled Receptors and Ischemic Stroke: a Focus on Molecular Function and Therapeutic Potential.Molecular neurobiology · 2021Review
- Small molecules targeting cyclooxygenase/prostanoid cascade in experimental brain ischemia: Do they translate?Medicinal research reviews · 2021Review
- Cannabidiol and Neurodevelopmental Disorders in Children.Frontiers in psychiatry · 2021Review
- Prostaglandins as the Agents That Modulate the Course of Brain Disorders.Degenerative neurological and neuromuscular disease · 2020Review
- The Interplay between the Endocannabinoid System, Epilepsy and Cannabinoids.International journal of molecular sciences · 2019Review
- The COX-2/prostanoid signaling cascades in seizure disorders.Expert opinion on therapeutic targets · 2019Review
- Genetic Deletion of PGFFrontiers in neuroscience · 2018Article
- Excitotoxicity-induced prostaglandin DJournal of lipid research · 2017Article
- Pathophysiological Roles of Cyclooxygenases and Prostaglandins in the Central Nervous System.Molecular neurobiology · 2016Review
- Hippocampal neuronal cyclooxygenase-2 downstream signaling imbalance in a rat model of chronic aluminium gluconate administration.Behavioral and brain functions : BBF · 2015Article
- Rapid and simultaneous quantitation of prostanoids by UPLC-MS/MS in rat brain.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2014Article
- Article
- Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury.Journal of neuroinflammation · 2013Article
- Prostaglandin FP receptor inhibitor reduces ischemic brain damage and neurotoxicity.Neurobiology of disease · 2012Article
- Putative role of prostaglandin receptor in intracerebral hemorrhage.Frontiers in neurology · 2012Article
- Role of prostaglandins in neuroinflammatory and neurodegenerative diseases.Mediators of inflammation · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Although some of the COX-2 metabolites and prostaglandins have been implicated in stroke and excitotoxicity, the role of prostaglandin F(2alpha) (PGF(2alpha)) and its FP receptor have not been elucidated in the pathogenesis of ischemic-reperfusion (I/R) brain injury. Here we investigated the FP receptor's contribution in a unilateral middle cerebral artery (MCA) occlusion model of focal cerebral ischemia in mice. The MCA in wild type (WT) and FP knockout (FP(-/-)) C57BL/6 male mice was transiently occluded with a monofilament for 90 min. After 96 h of reperfusion, the FP(-/-) mice had 25.3% less neurological deficit (P < 0.05) and 34.4% smaller infarct volumes (P < 0.05) than those of the WT mice. In a separate cohort, physiological parameters were monitored before, during, and after ischemia, and the results revealed no differences between the groups. Because excitotoxicity is an acute mediator of stroke outcome, the effect of acute NMDA-induced neurotoxicity was also tested. Forty-eight hours after unilateral intrastriatal NMDA injection, excitotoxic brain damage was 20.8% less extensive in the FP(-/-) mice (P < 0.05) than in the WT counterparts, further supporting the toxic contribution of the FP receptor in I/R injury. Additionally, we investigated the effect of post-treatment with the FP agonist latanoprost in mice subjected to MCA occlusion; such treatment resulted in an increase in neurological deficit and infarct size in WT mice (P < 0.05), though no effects were observed in the latanoprost-treated FP(-/-) mice. Together, the results suggest that the PGF(2alpha) FP receptor significantly enhances cerebral ischemic and excitotoxic brain injury and that these results are of importance when planning for potential development of therapeutic drugs to treat stroke and its acute and/or long term consequences.
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Registered trials
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