Expression of MCP-1 in the hippocampus of SHRSP with ischemia-related delayed neuronal death

Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):823-31. doi: 10.1007/s10571-006-9077-1. Epub 2006 Jun 7.

Abstract

1. The expression of monocyte chemoattractant protein-1 (MCP-1) was examined in stroke-prone spontaneously hypertensive rats with transient global ischemia in order to study the involvement of the infiltration of blood monocytes in the mechanism of ischemia-related neuronal death. 2. The brains of the animals with occlusion of the bilateral carotid arteries for 10 min were removed at 8 h, 1, 2, 4 and 7 days after reperfusion. Frozen sections were used for in situ hybridization and tissue specimens from the hippocampus and the cerebral cortex were used to measure the concentration of MCP-1 by ELISA. 3. No MCP-1 mRNA was detected in the hippocampus of the sham group animals. One day after ischemia-reperfusion, MCP-1 mRNA was clearly expressed in the CA4 subfield and the molecular layer of the dentate gyrus, while it was slightly expressed in the lacnosum moleculare of the CA1 subfield. A dramatic expression was demonstrated in the entire CA1 subfield at 2 days after the operation. Most of the cells expressing MCP-1 were astrocytes. At 4 and 7 days after reperfusion, no MCP-1 mRNA was detected in the hippocampus. The concentration of MCP-1 protein dramatically increased in the hippocampus at 2 days after reperfusion. 4. Taken together with the findings of our previous study showing an increased permeability of the blood-brain barrier in the hippocampus from 12 h after ischemia-reperfusion, the astrocytes expressing MCP-1 might therefore induce the migration of monocytes into the brain parenchyma. As a result, such astrocytes expressing MCP-1 may therefore be related to the pathological events of delayed neuronal death in the pyramidal neurons.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Ischemia / metabolism
  • Brain Ischemia / pathology*
  • Carotid Artery, Common / pathology
  • Cell Death
  • Chemokine CCL2 / metabolism*
  • Hippocampus / blood supply
  • Hippocampus / metabolism*
  • Hippocampus / pathology
  • Male
  • Neurons / metabolism
  • Neurons / pathology*
  • Neurons / physiology
  • Rats
  • Rats, Inbred SHR
  • Stroke / complications
  • Stroke / metabolism

Substances

  • Ccl2 protein, rat
  • Chemokine CCL2