Journal
NEUROSCIENCE LETTERS
Volume 441, Issue 1, Pages 120-124Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2008.05.080
Keywords
ischemia; preconditioning; protein kinase C; cerebral blood flow
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Funding
- NINDS NIH HHS [R01 NS040516-09, R01 NS044350-04, R01 NS044350-03, R01 NS044350, R01 NS040516, R01 NS044350-02] Funding Source: Medline
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In response to mild ischemic stress, the brain elicits endogenous survival mechanisms to protect cells against a subsequent lethal ischemic stress, referred to as ischemic tolerance. The molecular signals that mediate this protection are thought to involve the expression and activation of multiple kinases including protein kinase C (PKC). Here we demonstrate that epsilon PKC mediates cerebral ischemic tolerance in vivo. Systemic delivery of psi epsilon RACK, an epsilon PKC-selective peptide activator, confers neuroprotection against a subsequent cerebral ischemic event when delivered immediately prior to stroke. In addition, activation of epsilon PKC by psi epsilon RACK treatment decreases vascular tone in vivo, as demonstrated by a reduction in microvascular cerebral blood flow. Here we demonstrate the role of acute and transient epsilon PKC in early cerebral tolerance in vivo and suggest that extra-parenchymal mechanisms, such as vasoconstriction, may contribute to the conferred protection. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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