Abstract
Stroke is a devastating neurologic disease and a leading cause of death and disability worldwide. Thrombolytic agents have been used to re-establish circulation in thromboembolic stroke, but their utility is limited by hemorrhage and reperfusion injury. Studies with experimental stroke models, mouse genetics, and selective peptide inhibitors and activators have implicated protein kinase C (PKC) epsilon in ischemic preconditioning and PKCdelta and gamma in tissue injury. PKCdelta, resident both in neutrophils and in the brain, appears particularly essential for reperfusion injury, and recent work using PKCdelta-specific peptide inhibitors suggests that PKCdelta inhibitors could prove useful in attenuating reperfusion injury and improving outcome following thrombolysis.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Enzyme Inhibitors / therapeutic use
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Ischemic Preconditioning
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Isoenzymes / antagonists & inhibitors
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Isoenzymes / metabolism
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Mice
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Models, Biological
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / metabolism*
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Protein Kinase C-delta / antagonists & inhibitors
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Protein Kinase C-delta / metabolism
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Protein Kinase C-epsilon / genetics
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Protein Kinase C-epsilon / metabolism
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Rats
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Reperfusion Injury / enzymology*
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Reperfusion Injury / prevention & control
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Stroke / drug therapy
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Stroke / enzymology*
Substances
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Enzyme Inhibitors
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Isoenzymes
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protein kinase C gamma
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Protein Kinase C
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Protein Kinase C-delta
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Protein Kinase C-epsilon