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

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.

• Authors: Hiroshi Akiyama, Toru Nakazawa, Masahiko Shimura, Hiroshi Tomita, Makoto Tamai
• Journal: Neuroreport (Neuroreport) Vol. 13 Issue 16 Pg. 2103-7 (Nov 15 2002) ISSN: 0959-4965 [Print] England
• PMID: 12438934 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

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

Topics

• 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, pathology)
• Retinal Ganglion Cells (enzymology, pathology)
• Time Factors
• Up-Regulation (drug effects)