ArticleNeurotoxicology2013
Prostaglandin D2 toxicity in primary neurons is mediated through its bioactive cyclopentenone metabolites.
Article in Neurotoxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 39 citations in OpenAlex.
- Structural insights into the mechanism of activation and inhibition of the prostaglandin D2 receptor 1.Nature communications · 2025Article
- Exogenous prostaglandin DFrontiers in veterinary science · 2025Article
- Present State and Future Perspectives of Prostaglandins as a Differentiation Factor in Motor Neurons.Cellular and molecular neurobiology · 2022Review
- Roles of EP Receptors in the Regulation of Fluid Balance and Blood Pressure.Frontiers in endocrinology · 2022Review
- Article
- The Role of Eicosanoids in Alzheimer's Disease.International journal of environmental research and public health · 2019Review
- Review
- Role of UCHL1 in axonal injury and functional recovery after cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Prostaglandin D2/J2 signaling pathway in a rat model of neuroinflammation displaying progressive parkinsonian-like pathology: potential novel therapeutic targets.Journal of neuroinflammation · 2018Article
- Inflammatory signaling and metabolic regulation by nitro-fatty acids.Nitric oxide : biology and chemistry · 2018Review
- Physiological and Pathological Roles of 15-Deoxy-ΔMolecular neurobiology · 2018Review
- Electrophilic fatty acid nitroalkenes regulate Nrf2 and NF-κB signaling:A medicinal chemistry investigation of structure-function relationships.Scientific reports · 2018Article
- Prostaglandin J2 promotes O-GlcNAcylation raising APP processing by α- and β-secretases: relevance to Alzheimer's disease.Neurobiology of aging · 2018Article
- Regulation of inflammation by lipid mediators in oral diseases.Oral diseases · 2017Review
- Neurotoxic mechanisms by which the USP14 inhibitor IU1 depletes ubiquitinated proteins and Tau in rat cerebral cortical neurons: Relevance to Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Excitotoxicity-induced prostaglandin DJournal of lipid research · 2017Article
- Life and death in the trash heap: The ubiquitin proteasome pathway and UCHL1 in brain aging, neurodegenerative disease and cerebral Ischemia.Ageing research reviews · 2017Review
- Pathophysiological Roles of Cyclooxygenases and Prostaglandins in the Central Nervous System.Molecular neurobiology · 2016Review
- Prostaglandin J2: a potential target for halting inflammation-induced neurodegeneration.Annals of the New York Academy of Sciences · 2016Review
- A Plasma α-Tocopherome Can Be Identified from Proteins Associated with Vitamin E Status in School-Aged Children of Nepal.The Journal of nutrition · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Prostaglandin D2 (PGD2) is the most abundant prostaglandin in brain but its effect on neuronal cell death is complex and not completely understood. PGD2 may modulate neuronal cell death via activation of DP receptors or its metabolism to the cyclopentenone prostaglandins (CyPGs) PGJ2, Δ(12)-PGJ2 and 15-deoxy-Δ(12,14)-PGJ2, inducing cell death independently of prostaglandin receptors. This study aims to elucidate the effect of PGD2 on neuronal cell death and its underlying mechanisms. PGD2 dose-dependently induced cell death in rat primary neuron-enriched cultures in concentrations of ≥10μM, and this effect was not reversed by treatment with either DP1 or DP2 receptor antagonists. Antioxidants N-acetylcysteine (NAC) and glutathione which contain sulfhydryl groups that can bind to CyPGs, but not ascorbate or tocopherol, attenuated PGD2-induced cell death. Conversion of PGD2 to CyPGs was detected in neuronal culture medium; treatment with these CyPG metabolites alone exhibited effects similar to those of PGD2, including apoptotic neuronal cell death and accumulation of ubiquitinated proteins. Disruption of lipocalin-type prostaglandin D synthase (L-PGDS) protected neurons against hypoxia. These results support the hypothesis that PGD2 elicits its cytotoxic effects through its bioactive CyPG metabolites rather than DP receptor activation in primary neuronal culture.
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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.