Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury

Jonathan W. Nelson, Wenri Zhang, Nabil J. Alkayed, Ines P. Koerner

Research output: Contribution to journalArticle

2 Scopus citations

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 languageEnglish (US)
Pages (from-to)1416-1420
Number of pages5
JournalJournal of Cerebral Blood Flow and Metabolism
Volume35
Issue number9
DOIs
StatePublished - 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

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