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Hypoxic Preconditioning-Induced Cerebral Ischemic Tolerance
Author(s) -
Bradley K. Wacker,
Tae Sung Park,
Jeffrey M. Gidday
Publication year - 2009
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.109.560714
Subject(s) - sphingosine 1 phosphate , medicine , sphingosine , ischemia , sphingosine kinase , hypoxia (environmental) , pharmacology , stroke (engine) , lipid signaling , ischemic preconditioning , endocrinology , chemistry , receptor , mechanical engineering , organic chemistry , oxygen , engineering
The importance of bioactive lipid signaling under physiological and pathophysiological conditions is progressively becoming recognized. The disparate distribution of sphingosine kinase (SphK) isoform activity in normal and ischemic brain, particularly the large excess of SphK2 in cerebral microvascular endothelial cells, suggests potentially unique cell- and region-specific signaling by its product sphingosine-1-phosphate. The present study sought to test the isoform-specific role of SphK as a trigger of hypoxic preconditioning (HPC)-induced ischemic tolerance.

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