PMID- 10380894
OWN - NLM
STAT- MEDLINE
DCOM- 19990629
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 65
IP  - 6
DP  - 1999 Jun
TI  - Differential production of MCP-1 and cytokine-induced neutrophil chemoattractant 
      in the ischemic brain after transient focal ischemia in rats.
PG  - 744-9
AB  - Chemokines have been shown to play an important role in leukocyte infiltration 
      into ischemic lesions. Recently, the increased expression of monocyte 
      chemoattractant protein-1 (MCP-1) and cytokine-induced neutrophil chemoattractant 
      (CINC) was observed in experimental stroke models where infiltrated leukocytes 
      were supposed to induce tissue injury, however, the protein level and time course 
      of these chemokines have not been fully elucidated. Therefore, we analyzed the 
      time-dependent production of MCP-1 and CINC in the rat brain after transient 
      middle cerebral artery occlusion (MCAO) by means of specific enzyme-linked 
      immunosorbent assay systems. The MCP-1 levels in the ipsilateral hemispheres 
      increased from 6 h, peaked at 2 days, and thereafter gradually decreased. The 
      peak MCP-1 concentration was 89.2+/-28.2 ng/g tissue wet weight (mean +/- SEM, n 
      = 5, 49.3-fold greater than the contralateral value at the same time, P < 0.05), 
      which is supposed to be high enough to exert its biological effects. In contrast, 
      the maximum CINC concentration that corresponded to 2.9+/-0.7 ng/g tissue wet 
      weight (mean +/- SEM, n = 5, 55.0-fold greater than the contralateral value at 
      the same time, P < 0.05), was observed at 6 h. In addition, we confirmed the 
      temporal profile of leukocyte subtypes that infiltrated into the ischemic brain, 
      thus, neutrophil infiltration occurred at early stages (1-3 days), followed by 
      massive infiltration of macrophages at later stages (2-7 days). These studies 
      suggest that MCP-1 in cerebral ischemia actually plays a significant role in the 
      migration of macrophages into the lesion and that the differential temporal 
      production of these chemokines contributes to the regulation of infiltrated 
      leukocyte subtypes.
FAU - Yamagami, S
AU  - Yamagami S
AD  - Teijin Institute for Bio-Medical Research, Tokyo, Japan. s.yamagami@teijin.co.jp
FAU - Tamura, M
AU  - Tamura M
FAU - Hayashi, M
AU  - Hayashi M
FAU - Endo, N
AU  - Endo N
FAU - Tanabe, H
AU  - Tanabe H
FAU - Katsuura, Y
AU  - Katsuura Y
FAU - Komoriya, K
AU  - Komoriya K
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Growth Substances)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/*metabolism
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemokines, CXC/metabolism
MH  - Chemotactic Factors/*biosynthesis
MH  - Disease Models, Animal
MH  - Growth Substances/*biosynthesis
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Ischemic Attack, Transient/*complications
MH  - Leukocytes/cytology
MH  - Macrophages/cytology
MH  - Male
MH  - Rats
MH  - Rats, Wistar
EDAT- 1999/06/25 00:00
MHDA- 1999/06/25 00:01
CRDT- 1999/06/25 00:00
PHST- 1999/06/25 00:00 [pubmed]
PHST- 1999/06/25 00:01 [medline]
PHST- 1999/06/25 00:00 [entrez]
AID - 10.1002/jlb.65.6.744 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1999 Jun;65(6):744-9. doi: 10.1002/jlb.65.6.744.