PMID- 7860708
OWN - NLM
STAT- MEDLINE
DCOM- 19950323
LR  - 20190825
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 56
IP  - 2
DP  - 1995 Feb
TI  - Expression of monocyte chemoattractant protein-1 and macrophage inflammatory 
      protein-1 after focal cerebral ischemia in the rat.
PG  - 127-34
AB  - Chemoattractant cytokines, the chemokines, play an important role in early events 
      of inflammation at the site of tissue damage. We examined the expression of mRNA 
      and the protein products of two such chemokines; i.e. monocyte chemoattractant 
      protein-1 (MCP-1) and macrophage inflammatory protein-1 alpha (MIP-1 alpha) in 
      the ischemic brain tissue following middle cerebral artery occlusion (MCAo). The 
      mRNA transcripts of MCP-1 and MIP-1 alpha were detected by Northern hybridization 
      and reverse transcriptase polymerase chain reaction (RT/PCR), respectively, and 
      the anatomic distribution of specific proteins was analyzed by 
      immunohistochemistry. We found that MCP-1 mRNA was not expressed in the brains of 
      normal rats or rats sacrificed 2 h after MCAo. 6 h after the induction of 
      cerebral ischemia, weak expression of both mRNAs was detected in the ischemic 
      tissue. mRNAs were expressed up to 48 h, and were markedly attenuated at 96 h. In 
      the rats subjected to MCA occlusion, MCP-1 immunoreactivity was diffusely 
      expressed and localized to the ischemic area, and was most intense at 48 h after 
      MCA occlusion. Endothelial cells and macrophage-like cells expressed MCP-1 
      protein in the ischemic brain. The distribution and morphology of MIP-1 alpha 
      immunoreactive cells were identical with activated astrocytes. We conclude that 
      MCP-1 and MIP-1 alpha mRNAs and proteins are induced after cerebral ischemia in 
      the rat. They may have a role in promoting inflammatory and/or repair processes 
      in the ischemic brain, possibly by attracting or modulating inflammatory cells in 
      the ischemic area.
FAU - Kim, J S
AU  - Kim JS
AD  - Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South 
      Korea.
FAU - Gautam, S C
AU  - Gautam SC
FAU - Chopp, M
AU  - Chopp M
FAU - Zaloga, C
AU  - Zaloga C
FAU - Jones, M L
AU  - Jones ML
FAU - Ward, P A
AU  - Ward PA
FAU - Welch, K M
AU  - Welch KM
LA  - eng
GR  - P01 NS23393/NS/NINDS NIH HHS/United States
GR  - R01NS29463/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Brain Ischemia/*metabolism
MH  - Chemokine CCL2
MH  - Chemokine CCL4
MH  - Chemotactic Factors/*analysis/genetics/immunology
MH  - Cytokines/*analysis/genetics/immunology
MH  - Immunohistochemistry
MH  - Macrophage Inflammatory Proteins
MH  - Male
MH  - Molecular Sequence Data
MH  - Monokines/*analysis/genetics/immunology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Wistar
EDAT- 1995/02/01 00:00
MHDA- 2000/06/01 09:00
CRDT- 1995/02/01 00:00
PHST- 1995/02/01 00:00 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1995/02/01 00:00 [entrez]
AID - 016557289400138E [pii]
AID - 10.1016/0165-5728(94)00138-e [doi]
PST - ppublish
SO  - J Neuroimmunol. 1995 Feb;56(2):127-34. doi: 10.1016/0165-5728(94)00138-e.