ArticleJournal of neuroinflammation2011
Expression and cellular localization of cyclooxygenases and prostaglandin E synthases in the hemorrhagic brain.
Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 67 citations in OpenAlex.
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- Cannabidiol alleviates the inflammatory response in rats with traumatic brain injury through the PGEActa biochimica et biophysica Sinica · 2025Article
- New targets in spontaneous intracerebral hemorrhage.Current opinion in neurology · 2025Review
- Reactive spinal glia convert 2-AG to prostaglandins to drive aberrant astroglial calcium signaling.Frontiers in cellular neuroscience · 2024Article
- Network Pharmacology Prediction and Experimental Verification for Anti-Ferroptosis of Edaravone After Experimental Intracerebral Hemorrhage.Molecular neurobiology · 2023Article
- Lymphocyte-Related Immunomodulatory Therapy with Siponimod (BAF-312) Improves Outcomes in Mice with Acute Intracerebral Hemorrhage.Aging and disease · 2023Article
- An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- PLPP/CIN-mediated NF2 S10 dephosphorylation distinctly regulates kainate-induced seizure susceptibility and neuronal death through PAK1-NF-κB-COX-2-PTGES2 signaling pathway.Journal of neuroinflammation · 2023Article
- Ferroptosis: Underlying mechanism and the crosstalk with other modes of neuronal death after intracerebral hemorrhage.Frontiers in cellular neuroscience · 2023Review
- Role and mechanism of ferroptosis in neurological diseases.Molecular metabolism · 2022Review
- Diet-Induced High Serum Levels of Trimethylamine-N-oxide Enhance the Cellular Inflammatory Response without Exacerbating Acute Intracerebral Hemorrhage Injury in Mice.Oxidative medicine and cellular longevity · 2022Article
- Very early environmental enrichment protects against apoptosis and improves functional recovery from hypoxic-ischemic brain injury.Frontiers in molecular neuroscience · 2022Article
- Psychiatric traits and intracerebral hemorrhage: A Mendelian randomization study.Frontiers in psychiatry · 2022Article
- Emerging therapeutic targets for cerebral edema.Expert opinion on therapeutic targets · 2021Review
- Targeting the miRNA-155/TNFSF10 network restrains inflammatory response in the retina in a mouse model of Alzheimer's disease.Cell death & disease · 2021Article
- Review
- History of Nonsteroidal Anti-inflammatory Drug Use and Functional Outcomes After Spontaneous Intracerebral Hemorrhage.Neurocritical care · 2021Article
- Selective Ferroptosis Inhibitor Liproxstatin-1 Attenuates Neurological Deficits and Neuroinflammation After Subarachnoid Hemorrhage.Neuroscience bulletin · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAlthough cyclooxygenases (COX) and prostaglandin E synthases (PGES) have been implicated in ischemic stroke injury, little is known about their role in intracerebral hemorrhage (ICH)-induced brain damage. This study examines the expression and cellular localization of COX-1, COX-2, microsomal PGES-1 (mPGES-1), mPGES-2, and cytosolic PGES (cPGES) in mice that have undergone hemorrhagic brain injury.
methodsICH was induced in C57BL/6 mice by intrastriatal injection of collagenase. Expression and cellular localization of COX-1, COX-2, mPGES-1, mPGES-2, and cPGES were examined by immunofluorescence staining.
resultsIn the hemorrhagic brain, COX-1, mPGES-2, and cPGES were expressed constitutively in neurons; COX-1 was also constitutively expressed in microglia. The immunoreactivity of COX-2 was increased in neurons and astrocytes surrounding blood vessels at 5 h and then tended to decrease in neurons and increase in astrocytes at 1 day. At 3 days after ICH, COX-2 was observed primarily in astrocytes but was absent in neurons. Interestingly, the immunoreactivity of mPGES-1 was increased in neurons in the ipsilateral cortex and astrocytes in the ipsilateral striatum at 1 day post-ICH; the immunoreactivity of astrocytic mPGES-1 further increased at 3 days.
conclusionOur data suggest that microglial COX-1, neuronal COX-2, and astrocytic COX-2 and mPGES-1 may work sequentially to affect ICH outcomes. These findings have implications for efforts to develop anti-inflammatory strategies that target COX/PGES pathways to reduce ICH-induced secondary brain damage.
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Registered trials
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