Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury

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

doi:10.1038/jcbfm.2015.159

Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury

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

Anesthesiology & Perioperative Medicine

Research output: Contribution to journal › Article

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 language	English (US)
Pages (from-to)	1416-1420
Number of pages	5
Journal	Journal of Cerebral Blood Flow and Metabolism
Volume	35
Issue number	9
DOIs	https://doi.org/10.1038/jcbfm.2015.159
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

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Nelson, J. W., Zhang, W., Alkayed, N. J., & Koerner, I. P. (2015). Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury. Journal of Cerebral Blood Flow and Metabolism, 35(9), 1416-1420. https://doi.org/10.1038/jcbfm.2015.159

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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.",

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