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 | |
| State | Published - Sep 3 2015 |
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Keywords
- neuroprotection
- peroxisome
- single-nucleotide polymorphism
- soluble epoxide hydrolase
- TAT-fusion protein
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Clinical Neurology
- Neurology
Cite this
Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury. / Nelson, Jonathan W.; Zhang, Wenri; Alkayed, Nabil; Koerner, Ines.
In: Journal of Cerebral Blood Flow and Metabolism, Vol. 35, No. 9, 03.09.2015, p. 1416-1420.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Peroxisomal translocation of soluble epoxide hydrolase protects against ischemic stroke injury
AU - Nelson, Jonathan W.
AU - Zhang, Wenri
AU - Alkayed, Nabil
AU - Koerner, Ines
PY - 2015/9/3
Y1 - 2015/9/3
N2 - 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.
AB - 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.
KW - neuroprotection
KW - peroxisome
KW - single-nucleotide polymorphism
KW - soluble epoxide hydrolase
KW - TAT-fusion protein
UR - http://www.scopus.com/inward/record.url?scp=84940718545&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84940718545&partnerID=8YFLogxK
U2 - 10.1038/jcbfm.2015.159
DO - 10.1038/jcbfm.2015.159
M3 - Article
C2 - 26126869
AN - SCOPUS:84940718545
VL - 35
SP - 1416
EP - 1420
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 9
ER -