Presence of mitogen-activated protein kinase in retinal Müller cells and its neuroprotective effect ischemia-reperfusion injury

Neuroreport. 2002 Nov 15;13(16):2103-7. doi: 10.1097/00001756-200211150-00022.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Butadienes / pharmacology
  • Cell Death
  • Down-Regulation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Immunohistochemistry
  • MAP Kinase Signaling System / drug effects
  • Male
  • Mitogen-Activated Protein Kinases / metabolism*
  • Neuroglia / metabolism
  • Neuroprotective Agents / metabolism*
  • Nitriles / pharmacology
  • Phosphorylation / drug effects
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / enzymology*
  • Retina / enzymology*
  • Retina / pathology*
  • Retinal Ganglion Cells / enzymology
  • Retinal Ganglion Cells / pathology
  • Time Factors
  • Up-Regulation / drug effects

Substances

  • Butadienes
  • Enzyme Inhibitors
  • Neuroprotective Agents
  • Nitriles
  • U 0126
  • Mitogen-Activated Protein Kinases