ArticleNeurotoxicity research2013
Increased generation of cyclopentenone prostaglandins after brain ischemia and their role in aggregation of ubiquitinated proteins in neurons.
Article in Neurotoxicity research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Mirtazapine Induces Lipocalin-Type Prostaglandin D Synthase Expression in Brain Pericytes.Biomolecules · 2026Article
- Shared metabolomic signatures for prognostic precision across brain injuries.Brain & spine · 2025Article
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- Blood Markers in Relation to a History of Traumatic Brain Injury Across Stages of Cognitive Impairment in a Diverse Cohort.Journal of Alzheimer's disease : JAD · 2024Article
- Role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury.Ageing research reviews · 2023Review
- Chlorogenic acid modulates the ubiquitin-proteasome system in stroke animal model.Laboratory animal research · 2022Article
- Timapiprant, a prostaglandin D2 receptor antagonist, ameliorates pathology in a rat Alzheimer's model.Life science alliance · 2022Article
- Article
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- PACAP27 mitigates an age-dependent hippocampal vulnerability to PGJ2-induced spatial learning deficits and neuroinflammation in mice.Brain and behavior · 2020Article
- Mitochondrial and calcium perturbations in rat CNS neurons induce calpain-cleavage of Parkin: Phosphatase inhibition stabilizes pSerBiochimica et biophysica acta. Molecular basis of disease · 2019Article
- 15-Deoxy-ΔThe Journal of biological chemistry · 2019Article
- 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 J2 promotes O-GlcNAcylation raising APP processing by α- and β-secretases: relevance to Alzheimer's disease.Neurobiology of aging · 2018Article
- 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
- 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
- Modification of ubiquitin C-terminal hydrolase L1 by reactive lipid species: role in neural regeneration and diseases of aging.Neural regeneration research · 2016Article
- Prostaglandin J2: a potential target for halting inflammation-induced neurodegeneration.Annals of the New York Academy of Sciences · 2016Review
- The point mutation UCH-L1 C152A protects primary neurons against cyclopentenone prostaglandin-induced cytotoxicity: implications for post-ischemic neuronal injury.Cell death & disease · 2015Article
- Protein disulfide isomerase as a novel target for cyclopentenone prostaglandins: implications for hypoxic ischemic injury.The FEBS journal · 2015Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The cyclopentenone prostaglandin (CyPG) J₂ series, including prostaglandin J₂ (PGJ₂), Δ¹²-PGJ₂, and 15-deoxy-∆¹²,¹⁴-prostaglandin J₂ (15d-PGJ₂), are active metabolites of PGD₂, exerting multiple effects on neuronal function. However, the physiologic relevance of these effects remains uncertain as brain concentrations of CyPGs have not been precisely determined. In this study, we found that free PGD₂ and the J₂ series CyPGs (PGJ₂, Δ¹²-PGJ₂, and 15d-PGJ₂) were increased in post-ischemic rat brain as detected by UPLC-MS/MS with 15d-PGJ₂ being the most abundant CyPG. These increases were attenuated by pre-treating with the cyclooxygenase (COX) inhibitor piroxicam. Next, effects of chronic exposure to 15d-PGJ₂ were examined by treating primary neurons with 15d-PGJ₂, CAY10410 (a 15d-PGJ₂ analog lacking the cyclopentenone ring structure), or vehicle for 24 to 96 h. Because we found that the concentration of free 15d-PGJ₂ decreased rapidly in cell culture medium, freshly prepared medium containing 15d-PGJ₂, CAY10410, or vehicle was changed twice daily to maintain steady extracellular concentrations. Incubation with 2.5 μM 15d-PGJ₂, but not CAY10410, increased the neuronal cell death without the induction of caspase-3 or PARP cleavage, consistent with a primarily necrotic mechanism for 15d-PGJ₂-induced cell death which was further supported by TUNEL assay results. Ubiquitinated protein accumulation and aggregation was observed after 96 h 15d-PGJ₂ incubation, accompanied by compromised 20S proteasome activity. Unlike another proteasome inhibitor, MG132, 15d-PGJ₂ treatment did not activate autophagy or induce aggresome formation. Therefore, the cumulative cytotoxic effects of increased generation of CyPGs after stroke may contribute to delayed post-ischemic neuronal injury.
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