Extracellular signal-regulated kinase involved in NGF/VEGF-induced neuroprotective effect

Neurosci Lett. 2008 Mar 28;434(2):212-7. doi: 10.1016/j.neulet.2008.01.078. Epub 2008 Feb 13.

Abstract

Compelling evidence has shown that extracellular signal-regulated kinase (ERK) is widely expressed in many tissues, including the brain. In the present work, we investigated the temporospatial alterations of ERK1 immunoreactivity in hippocampus and perifocal cortex, and the expression involved in NGF/VEGF-induced neuroprotective effect. We demonstrated that ERK1 expression was first increased in hippocampal CA3/DG 1 h after reperfusion, then it was also increased 6 h after reperfusion in other brain regions, with a peak at day 1-3, and then gradually decreased to basal level at day 14. The expression of caspase-3 was strongly increased 1 h after reperfusion, with peak demonstrated at 3d. NGF/VEGF significantly inhibited the expression of ERK1 and caspase-3. These results suggest that ERK1 signaling pathway may be involved in neuronal cell death and NGF/VEGF-induced neuroprotective effect and there appeared an association between ERK and caspase-3. Inhibition of the ERK signaling pathway might therefore provide an efficient way to prevent neuronal cell death after ischemic cerebral injuries.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Brain Ischemia / drug therapy*
  • Brain Ischemia / metabolism*
  • Brain Ischemia / pathology
  • Caspase 3 / metabolism
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Infarction, Middle Cerebral Artery / metabolism
  • Infarction, Middle Cerebral Artery / pathology
  • Male
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Nerve Growth Factor / metabolism
  • Nerve Growth Factor / pharmacology*
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / pharmacology*
  • Rabbits
  • Reperfusion Injury / drug therapy
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Vascular Endothelial Growth Factor A / metabolism
  • Vascular Endothelial Growth Factor A / pharmacology*

Substances

  • Neuroprotective Agents
  • Vascular Endothelial Growth Factor A
  • Nerve Growth Factor
  • Mitogen-Activated Protein Kinase 3
  • Caspase 3