ArticleBritish journal of pharmacology2010
Microsomal prostaglandin E synthase-1 and cyclooxygenase-2 are both required for ischaemic excitotoxicity.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Scientific reports · 2016Pooled it
- HIV-1 Tat Upregulates TREM1 Expression in Human Microglia.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Novel, Brain-Permeable, Cross-Species Benzothiazole Inhibitors of Microsomal Prostaglandin E Synthase-1 (mPGES-1) Dampen NeuroinflammationACS pharmacology & translational science · 2023Article
- Therapeutic Potentials of MicroRNA-126 in Cerebral Ischemia.Molecular neurobiology · 2023Review
- Transient inhibition of microsomal prostaglandin E synthase-1 after status epilepticus blunts brain inflammation and is neuroprotective.Molecular brain · 2023Article
- Article
- COX-2/PGE2 Pathway Inhibits the Ferroptosis Induced by Cerebral Ischemia Reperfusion.Molecular neurobiology · 2022Article
- Inducible Prostaglandin E Synthase as a Pharmacological Target for Ischemic Stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Inhibition of Prostaglandin E2 Receptor EP3 Attenuates Oxidative Stress and Neuronal Apoptosis Partially by Modulating p38MAPK/FOXO3/Mul1/Mfn2 Pathway after Subarachnoid Hemorrhage in Rats.Oxidative medicine and cellular longevity · 2022Article
- Small molecules targeting cyclooxygenase/prostanoid cascade in experimental brain ischemia: Do they translate?Medicinal research reviews · 2021Review
- Prostaglandin E receptors as targets for ischemic stroke: Novel evidence and molecular mechanisms of efficacy.Pharmacological research · 2021Review
- Inhibition of human microsomal PGE2 synthase-1 reduces seizure-induced increases of P-glycoprotein expression and activity at the blood-brain barrier.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Alleviation of Microglial Activation Induced by p38 MAPK/MK2/PGEScientific reports · 2017Article
- Pathophysiological Roles of Cyclooxygenases and Prostaglandins in the Central Nervous System.Molecular neurobiology · 2016Review
- PGE2-EP3 signaling exacerbates intracerebral hemorrhage outcomes in 24-mo-old mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- Misoprostol Reverse Hippocampal Neuron Cyclooxygenase-2 Downstream Signaling Imbalance in Aluminum-Overload Rats.Current Alzheimer research · 2016Article
- The role of glutamate in neuronal ischemic injury: the role of spark in fire.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Review
- Natural plant products and extracts that reduce immunoexcitotoxicity-associated neurodegeneration and promote repair within the central nervous system.Surgical neurology international · 2012Article
- Expression and cellular localization of cyclooxygenases and prostaglandin E synthases in the hemorrhagic brain.Journal of neuroinflammation · 2011Article
- Microsomal prostaglandin E synthase-1 contributes to ischaemic excitotoxicity through prostaglandin E2 EP3 receptors.British journal of pharmacology · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAlthough both microsomal prostaglandin E synthase (mPGES)-1 and cyclooxygenase (COX)-2 are critical factors in stroke injury, but the interactions between these enzymes in the ischaemic brain is still obscure. This study examines the hypothesis that mPGES-1 activity is required for COX-2 to cause neuronal damage in ischaemic injury. EXPERIMENTAL APPROACH: We used a glutamate-induced excitotoxicity model in cultures of rat or mouse hippocampal slices and a mouse middle cerebral artery occlusion-reperfusion model in vivo. The effect of a COX-2 inhibitor on neuronal damage in mPGES-1 knockout (KO) mice was compared with that in wild-type (WT) mice. KEY
resultsIn rat hippocampal slices, glutamate-induced excitotoxicity, as well as prostaglandin (PG) E(2) production and PGES activation, was significantly attenuated by either MK-886 or NS-398, inhibitors of mPGES-1 and COX-2 respectively; however, co-application of these inhibitors had neither an additive nor a synergistic effect. The protective effect of NS-398 on the excitotoxicity observed in WT slices was completely abolished in mPGES-1 KO slices, which showed less excitotoxicity than WT slices. In the transient focal ischaemia model, mPGES-1 and COX-2 were co-localized in the infarct region of the cortex. Injection of NS-398 reduced not only ischaemic PGE(2) production, but also ischaemic injuries in WT mice, but not in mPGES-1 KO mice, which showed less dysfunction than WT mice. CONCLUSION AND IMPLICATIONS: Microsomal prostaglandin E synthase-1 and COX-2 are co-induced by excess glutamate in ischaemic brain. These enzymes are co-localized and act together to exacerbate stroke injury, by excessive PGE(2) production.
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