Abstract | BACKGROUND AND PURPOSE: METHODS: RESULTS:
Isoflurane preconditioning and hypoxia preconditioning significantly reduced infarct volume and improved neurological outcome in wild-type and SPK1(-/-) mice but not in SPK2(-/-) mice. Pretreatment with SKI-II or ABC294640 abolished the isoflurane preconditioning-induced tolerance. Western blot showed a rapid and sustained increase in SPK2 level, whereas SPK1 level was similar between preconditioned mice and controls. Hypoxia-inducible factor 1α was upregulated in wild-type isoflurane-preconditioned mice but not in SPK2(-/-). Isoflurane preconditioning protected primary neurons against cell death, which was abolished in ABC294640-treated cells. CONCLUSIONS: Applying genetic and pharmacological approaches, we demonstrate that neuronal SPK2 isoform plays an important role in cerebral preconditioning.
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Authors | Lai Ming Yung, Ying Wei, Tao Qin, Yumei Wang, Charles D Smith, Christian Waeber |
Journal | Stroke
(Stroke)
Vol. 43
Issue 1
Pg. 199-204
(Jan 2012)
ISSN: 1524-4628 [Electronic] United States |
PMID | 21980199
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Hif1a protein, mouse
- Hypoxia-Inducible Factor 1, alpha Subunit
- Phosphotransferases (Alcohol Group Acceptor)
- sphingosine kinase
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Topics |
- Animals
- Brain
(metabolism, pathology)
- Brain Ischemia
(metabolism, pathology)
- Hypoxia-Inducible Factor 1, alpha Subunit
(genetics, metabolism)
- Ischemic Preconditioning
(methods)
- Male
- Mice
- Mice, Knockout
- Neurons
(metabolism, pathology)
- Phosphotransferases (Alcohol Group Acceptor)
(genetics, metabolism)
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