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.
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