PMID- 14607260
OWN - NLM
STAT- MEDLINE
DCOM- 20040105
LR  - 20190701
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 74
IP  - 2-3
DP  - 2003 Dec 5
TI  - Chemokines and their receptors in the brain: pathophysiological roles in ischemic 
      brain injury.
PG  - 321-7
AB  - Chemokines constitute a large family of structurally-related small cytokines 
      originally identified as factors regulating the migration of leukocytes in 
      inflammatory and immune responses. Production of chemokines and their receptors 
      in the brain has been reported under various pathological conditions. We revealed 
      that mRNA expression for monocyte chemoattractant protein-1 (MCP-1) and 
      macrophage inflammatory protein-1alpha (MIP-1alpha), members of the CC 
      chemokines, was induced in the rat brain after focal cerebral ischemia, and that 
      intracerebroventricular injection of viral macrophage inflammatory protein-II 
      (vMIP-II), a broad-spectrum chemokine receptor antagonist, reduced infarct volume 
      in a dose-dependent manner. These findings suggest that brain chemokines are 
      involved in ischemic injury, and that chemokine receptors are potential targets 
      for therapeutic intervention in stroke. Another potential target to suppress the 
      harmful effect of chemokines is the signal transmission system(s) regulating the 
      chemokine production. However, very little is known about how the production of 
      chemokines is regulated in the ischemic brain. We examined the induction of MCP-1 
      production by excitotoxic injury via activation of NMDA receptors in the 
      cortico-striatal slice cultures, and found that excitotoxic injury induced MCP-1 
      production in the slice culture. Almost all of the MCP-1 immunoreactivity was 
      located on astrocytes. On the other hand, NMDA-treatment failed to increase the 
      MCP-1 production in the enriched astrocyte cultures, indicating that NMDA dose 
      not directly act on astrocytes. Some signal(s) is likely sent from the injured 
      neurons to astrocytes to induce the MCP-1 production. These results showed that 
      organotypic slice cultures are useful to investigate the molecular mechanism 
      regulating the chemokine production in the injured brain.
FAU - Minami, Masabumi
AU  - Minami M
AD  - Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, 
      Kyoto University, 606-8501, Kyoto, Japan.
FAU - Satoh, Masamichi
AU  - Satoh M
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Chemokines)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Brain Chemistry/drug effects/*physiology
MH  - Chemokines/biosynthesis/*physiology
MH  - Humans
MH  - Neuroprotective Agents/pharmacology/therapeutic use
MH  - Organ Culture Techniques
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Chemokine/antagonists & inhibitors/*physiology
MH  - Stroke/*physiopathology
RF  - 10
EDAT- 2003/11/11 05:00
MHDA- 2004/01/06 05:00
CRDT- 2003/11/11 05:00
PHST- 2003/11/11 05:00 [pubmed]
PHST- 2004/01/06 05:00 [medline]
PHST- 2003/11/11 05:00 [entrez]
AID - S0024320503008385 [pii]
AID - 10.1016/j.lfs.2003.09.019 [doi]
PST - ppublish
SO  - Life Sci. 2003 Dec 5;74(2-3):321-7. doi: 10.1016/j.lfs.2003.09.019.