ArticleProstaglandins & other lipid mediators
Altered behavioral phenotypes in soluble epoxide hydrolase knockout mice: effects of traumatic brain injury.
Article in Prostaglandins & other lipid mediators. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Inhibition of soluble epoxide hydrolase confers neuroprotection and restores microglial homeostasis in a tauopathy mouse model.Molecular neurodegeneration · 2025Article
- Proteomic analysis discovers potential biomarkers of early traumatic axonal injury in the brainstem.International journal of legal medicine · 2024Article
- Hyperglycemia disrupted the integrity of the blood-brain barrier following diffuse axonal injury through the sEH/NF-κB pathway.Immunity, inflammation and disease · 2023Article
- Enhancement of the liver's neuroprotective role ameliorates traumatic brain injury pathology.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Genetic Deletion of Soluble Epoxide Hydroxylase Causes Anxiety-Like Behaviors in Mice.Molecular neurobiology · 2019Article
- Humble beginnings with big goals: Small molecule soluble epoxide hydrolase inhibitors for treating CNS disorders.Progress in neurobiology · 2019Review
- Fatty acid chemical mediator provides insights into the pathology and treatment of Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- P450 Eicosanoids and Reactive Oxygen Species Interplay in Brain Injury and Neuroprotection.Antioxidants & redox signaling · 2018Article
- Article
- Cytochrome P450 eicosanoids in cerebrovascular function and disease.Pharmacology & therapeutics · 2017Review
- Possible role of Epoxyeicosatrienoic acid in prevention of oxidative stress mediated neuroinflammation in Parkinson disorders.Medical hypotheses · 2016Article
- A Compact Blast-Induced Traumatic Brain Injury Model in Mice.Journal of neuropathology and experimental neurology · 2016Article
- The Controlled Cortical Impact Model: Applications, Considerations for Researchers, and Future Directions.Frontiers in neurology · 2016Review
- Soluble epoxide hydrolase as an anti-inflammatory target of the thrombolytic stroke drug SMTP-7.The Journal of biological chemistry · 2014Article
- Traumatic brain injury using mouse models.Translational stroke research · 2014Review
- Review
- Temporal changes of cytochrome P450 (Cyp) and eicosanoid-related gene expression in the rat brain after traumatic brain injury.BMC genomics · 2013Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
After traumatic brain injury (TBI), arachidonic acid (ArA) is released from damaged cell membranes and metabolized to many bioactive eicosanoids, including several epoxyeicosatrienoic acids (EETs). Soluble epoxide hydrolase (Ephx2, sEH) appears to be the predominant pathway for EET metabolism to less active dihydroxyeicosatrienoates (DHETs). Prior studies indicate that brain levels of EETs increase transiently after TBI and EETs have antiinflammatory and neuroprotective activities which may benefit the injured brain. If the net effect of increased EET levels in the injured brain is beneficial to recovery, then Ephx2 gene disruption would be expected to enhance elevated EET levels and improve recovery in the injured brain. Thus, Ephx2-KO (Ephx2(-/-) bred onto pure C57Bl/6 background) mice were compared to wild-type controls in a unilateral controlled cortical impact model of TBI. Before injury, animals behaved comparably in open field activity and neurologic reflexes. Interestingly, the Ephx2-KO mice showed improved motor coordination on a beam walk task, yet showed indications of defective learning in a test of working spatial memory. After surgery, brain-injured Ephx2-KO mice again had less of a deficit in the beam walk than wild-type, and the difference in latency (post-pre) showed a trend of protection for Ephx2-KO mice after TBI. Brain-injured mice showed no genotype differences in working memory. Surprisingly, sham-operated Ephx2-KO mice exhibited an injured phenotype for working memory, compared to sham-operated wild-type mice. Brain eicosanoid levels were measured using liquid chromatography with tandem mass spectrometry. Of the 20 eicosanoids evaluated, only 8,9-EET was elevated in the Ephx2-KO cerebral cortex (37 d post-surgery, in both sham and injured). Tissue DHET levels were below the limit of quantification. These results reflect a significant contribution of sEH deficiency in coordination of ambulatory movements and working spatial memory in the mouse. Further investigation of differential sEH expression and EET levels at earlier time points and across other brain regions may shed light on these behavioral differences.
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