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ɛPKC confers acute tolerance to cerebral ischemic reperfusion injury

Authors
Journal
Neuroscience Letters
0304-3940
Publisher
Elsevier
Publication Date
Volume
441
Issue
1
Identifiers
DOI: 10.1016/j.neulet.2008.05.080
Keywords
  • Ischemia
  • Preconditioning
  • Protein Kinase C
  • Cerebral Blood Flow
Disciplines
  • Biology

Abstract

Abstract 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 ɛPKC mediates cerebral ischemic tolerance in vivo. Systemic delivery of ψɛRACK, an ɛPKC-selective peptide activator, confers neuroprotection against a subsequent cerebral ischemic event when delivered immediately prior to stroke. In addition, activation of ɛPKC by ψɛRACK 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 ɛPKC in early cerebral tolerance in vivo and suggest that extra-parenchymal mechanisms, such as vasoconstriction, may contribute to the conferred protection.

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