Abstract
Soluble epoxide hydrolase (sEH) contributes to cardiovascular disease, including stroke, although the exact mechanism remains unclear. While primarily a cytosolic enzyme, sEH can translocate into peroxisomes. The relevance of this for stroke injury is not understood. We tested the hypothesis that sEH-mediated injury is tied to the cytoplasmic localization. We found that a human sEH variant possessing increased affinity to peroxisomes reduced stroke injury in sEH-null mice, whereas infarcts were significantly larger when peroxisomal translocation of sEH was disrupted. We conclude that sEH contributes to stroke injury only when localized in the cytoplasm, while peroxisomal sEH may be protective.
Original language | English (US) |
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Pages (from-to) | 1416-1420 |
Number of pages | 5 |
Journal | Journal of Cerebral Blood Flow and Metabolism |
Volume | 35 |
Issue number | 9 |
DOIs | |
State | Published - Sep 3 2015 |
Keywords
- TAT-fusion protein
- neuroprotection
- peroxisome
- single-nucleotide polymorphism
- soluble epoxide hydrolase
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Cardiology and Cardiovascular Medicine