PMID- 16758320
OWN - NLM
STAT- MEDLINE
DCOM- 20070424
LR  - 20220409
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 26
IP  - 4-6
DP  - 2006 Jul-Aug
TI  - Expression of MCP-1 in the hippocampus of SHRSP with ischemia-related delayed 
      neuronal death.
PG  - 823-31
AB  - 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.
FAU - Sakurai-Yamashita, Yasuko
AU  - Sakurai-Yamashita Y
AD  - Department of Pharmacology, Nagasaki University Graduate School of Biomedical 
      Sciences, Nagasaki, 852-8523, Japan. yasukosy@net.nagasaki-u.ac.jp
FAU - Shigematsu, Kazuto
AU  - Shigematsu K
FAU - Yamashita, Kimihiro
AU  - Yamashita K
FAU - Niwa, Masami
AU  - Niwa M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060607
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/metabolism/*pathology
MH  - Carotid Artery, Common/pathology
MH  - Cell Death
MH  - Chemokine CCL2/*metabolism
MH  - Hippocampus/blood supply/*metabolism/pathology
MH  - Male
MH  - Neurons/metabolism/*pathology/physiology
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Stroke/complications/metabolism
EDAT- 2006/06/08 09:00
MHDA- 2007/04/25 09:00
CRDT- 2006/06/08 09:00
PHST- 2005/11/24 00:00 [received]
PHST- 2006/04/21 00:00 [accepted]
PHST- 2006/06/08 09:00 [pubmed]
PHST- 2007/04/25 09:00 [medline]
PHST- 2006/06/08 09:00 [entrez]
AID - 10.1007/s10571-006-9077-1 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):823-31. doi: 10.1007/s10571-006-9077-1. 
      Epub 2006 Jun 7.