Abstract
The purpose of this study was to determine whether the mitogen-activated protein kinase (MAPK) signaling pathway in the retina plays a neuroprotective role against ischemia- reperfusion injury. Western blot analysis showed that the MAPK activity was markedly increased within an hour after ischemia-reperfusion and subsequently decreased. Immunohistochemical studies revealed that MAPK was expressed mainly in the retinal Müller cells (RMCs). Pre-ischemic intravitreal administration of a MAPK inhibitor, U0126, increased the number of ganglion cell deaths induced by ischemia-reperfusion injury. We conclude that the MAPK activated in the RMCs protects ganglion cells against the ischemia-reperfusion injury through glia-neuronal interaction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Butadienes / pharmacology
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Cell Death
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Down-Regulation / drug effects
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Enzyme Inhibitors / pharmacology
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Immunohistochemistry
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MAP Kinase Signaling System / drug effects
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Male
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Mitogen-Activated Protein Kinases / metabolism*
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Neuroglia / metabolism
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Neuroprotective Agents / metabolism*
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Nitriles / pharmacology
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Phosphorylation / drug effects
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Rats
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Rats, Sprague-Dawley
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Reperfusion Injury / enzymology*
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Retina / enzymology*
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Retina / pathology*
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Retinal Ganglion Cells / enzymology
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Retinal Ganglion Cells / pathology
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Time Factors
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Up-Regulation / drug effects
Substances
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Butadienes
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Enzyme Inhibitors
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Neuroprotective Agents
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Nitriles
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U 0126
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Mitogen-Activated Protein Kinases