PMID- 19559679
OWN - NLM
STAT- MEDLINE
DCOM- 20090925
LR  - 20090821
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1289
DP  - 2009 Sep 15
TI  - The role of CC chemokine receptor 2 on microglia activation and blood-borne cell 
      recruitment after transient focal cerebral ischemia in mice.
PG  - 79-84
LID - 10.1016/j.brainres.2009.06.054 [doi]
AB  - The chemokine receptor 2 (CCR2) is involved in inflammatory reactions following 
      cerebral ischemia. Monocyte chemoattractant protein-1 (MCP-1) binds with high 
      affinity to CCR2. MCP-1 is necessary for recruiting blood-borne cells to the 
      injury site whereas it does not affect microglia activation and migration. 
      MCP-1-deficient mice develop smaller infarcts and show a better functional 
      outcome. CCR2-deficient mice also develop smaller infarcts and have a reduced 
      expression of inflammatory cytokines during reperfusion. In the present study we 
      investigated the differential role of inflammatory cells in CCR2-deficient mice, 
      using green fluorescent protein (GFP)-transgenic bone marrow chimeras. After 30 
      min of transient middle cerebral artery occlusion (MCAO), activation of local 
      microglia was similar in CCR2-deficient animals and their littermate controls 
      over the study period, whereas an influx of GFP-positive cells was diminished in 
      CCR2-deficient mice. Infiltrating macrophages were significantly reduced at day 
      seven in the deficient animals (26.04+/-25.19 cells/mm(2)) compared to control 
      mice (86.83+/-44.41 cells/mm(2), p<0.001). Neutrophils were also significantly 
      reduced in CCR2-deficient mice (83% on day 2, 76% on day 4 and 89% on day 7, 
      p<0.001). A significant reduction of infarct volume in CCR2-deficient animals 
      could not be detected. In this study a clear differentiation of local and 
      blood-borne inflammatory cell reaction after cerebral ischemia could be shown, 
      demonstrating that CCR2-deficiency attenuates hematogenous cell recruitment to 
      the injury site whereas microglia activation and migration is not affected.
FAU - Schilling, Matthias
AU  - Schilling M
AD  - Department of Neurology, University Hospital Munster, Albert-Schweitzer-Str. 33, 
      D-48129 Munster, Germany. schillim@uni-muenster.de
FAU - Strecker, Jan-Kolja
AU  - Strecker JK
FAU - Ringelstein, E Bernd
AU  - Ringelstein EB
FAU - Schabitz, Wolf-Rudiger
AU  - Schabitz WR
FAU - Kiefer, Reinhard
AU  - Kiefer R
LA  - eng
PT  - Journal Article
DEP - 20090624
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Receptors, CCR2)
SB  - IM
MH  - Animals
MH  - Bone Marrow/immunology
MH  - Immunohistochemistry
MH  - Ischemic Attack, Transient/*immunology/physiopathology
MH  - Macrophages/*immunology
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Microglia/*immunology
MH  - Neutrophil Infiltration
MH  - Neutrophils/*immunology
MH  - Receptors, CCR2/*immunology
MH  - Transplantation Chimera
EDAT- 2009/06/30 09:00
MHDA- 2009/09/26 06:00
CRDT- 2009/06/30 09:00
PHST- 2009/03/20 00:00 [received]
PHST- 2009/06/11 00:00 [revised]
PHST- 2009/06/16 00:00 [accepted]
PHST- 2009/06/30 09:00 [entrez]
PHST- 2009/06/30 09:00 [pubmed]
PHST- 2009/09/26 06:00 [medline]
AID - S0006-8993(09)01270-0 [pii]
AID - 10.1016/j.brainres.2009.06.054 [doi]
PST - ppublish
SO  - Brain Res. 2009 Sep 15;1289:79-84. doi: 10.1016/j.brainres.2009.06.054. Epub 2009 
      Jun 24.