PMID- 19374937
OWN - NLM
STAT- MEDLINE
DCOM- 20090824
LR  - 20220309
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 161
IP  - 3
DP  - 2009 Jul 7
TI  - Effects of monocyte chemoattractant protein 1 on blood-borne cell recruitment 
      after transient focal cerebral ischemia in mice.
PG  - 806-12
LID - 10.1016/j.neuroscience.2009.04.025 [doi]
AB  - Monocyte chemoattractant protein 1 (MCP-1) plays an important role in 
      inflammatory reactions following cerebral ischemia. It is known that MCP-1 
      overexpression leads to increased infarct volume and elevated hematogenous cell 
      recruitment, while MCP-1-deficient mice develop smaller infarcts. It was supposed 
      that MCP-1 dependent macrophage recruitment might be the underlying mechanism of 
      ischemic brain damage but a precise distinction of local microglia and invading 
      macrophages was not performed. In this study we investigated the differential 
      role of MCP-1 on inflammatory cells in MCP-1-deficient mice, using green 
      fluorescent protein (GFP) transgenic bone marrow chimeras. After 30-min of focal 
      cerebral ischemia microglia was rapidly activated and was not different between 
      MCP-1-deficient mice and wild type controls. Activated microglia outnumbered 
      GFP-positive macrophages over the study period. Furthermore, macrophage 
      infiltration was significantly reduced at day 7 in MCP-1-deficient animals 
      (31.2+/-20.1 cells/mm(2)) compared to MCP-1 wild type mice (131.5+/-66.7 
      cells/mm(2), P<0.001). Neutrophils were also significantly reduced in 
      MCP-1-deficient mice (62% on day 4% and 87% on day 7; P<0.001). This is the first 
      investigation in cerebral ischemia showing that MCP-1 is necessary for recruiting 
      blood-borne cells to the injury site whereas it does not affect the microglia 
      activation and migration. However, the remarkable predominance of activated 
      microglia and the additional attenuation of invading macrophages suggest that 
      different mechanisms than macrophage recruitment are responsible for the 
      MCP-1-mediated neuroprotective effects after experimental stroke.
FAU - Schilling, M
AU  - Schilling M
AD  - Department of Neurology, University Hospital Munster, Munster, Germany. 
      schillim@uni-muenster.de
FAU - Strecker, J-K
AU  - Strecker JK
FAU - Schabitz, W-R
AU  - Schabitz WR
FAU - Ringelstein, E B
AU  - Ringelstein EB
FAU - Kiefer, R
AU  - Kiefer R
LA  - eng
PT  - Journal Article
DEP - 20090415
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 147336-22-9 (Green Fluorescent Proteins)
SB  - IM
MH  - Animals
MH  - Brain/immunology/pathology
MH  - Brain Ischemia/*immunology/pathology
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Green Fluorescent Proteins/genetics
MH  - Immunohistochemistry
MH  - Ischemic Attack, Transient/*immunology/pathology
MH  - Macrophages/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Microglia/*physiology
MH  - Neutrophils/*physiology
MH  - Stroke/immunology/pathology
MH  - Transplantation Chimera
EDAT- 2009/04/21 09:00
MHDA- 2009/08/25 09:00
CRDT- 2009/04/21 09:00
PHST- 2009/01/22 00:00 [received]
PHST- 2009/03/18 00:00 [revised]
PHST- 2009/04/09 00:00 [accepted]
PHST- 2009/04/21 09:00 [entrez]
PHST- 2009/04/21 09:00 [pubmed]
PHST- 2009/08/25 09:00 [medline]
AID - S0306-4522(09)00630-7 [pii]
AID - 10.1016/j.neuroscience.2009.04.025 [doi]
PST - ppublish
SO  - Neuroscience. 2009 Jul 7;161(3):806-12. doi: 10.1016/j.neuroscience.2009.04.025. 
      Epub 2009 Apr 15.