PMID- 22031820
OWN - NLM
STAT- MEDLINE
DCOM- 20120529
LR  - 20211020
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 6
IP  - 10
DP  - 2011
TI  - Monocyte chemoattractant protein-1-deficiency impairs the expression of IL-6, 
      IL-1beta and G-CSF after transient focal ischemia in mice.
PG  - e25863
LID - 10.1371/journal.pone.0025863 [doi]
LID - e25863
AB  - Monocyte chemoattractant protein-1 (MCP-1), a chemokine secreted by neurons and 
      astrocytes following stroke is known to aggravate ischemia-related damage. 
      Previous studies revealed that MCP-1-deficient mice develop smaller infarcts and 
      have an improved neurological outcome, whereas mice overexpressing MCP-1 show 
      worsened brain damage and impaired neurological function. The aim of the present 
      study was to elucidate the molecular background of the enhanced recovery in 
      MCP-1-deficient mice after stroke. For this purpose, we (1) performed expression 
      analyses on crucial post-stroke related inflammatory genes in MCP-1-deficient 
      mice compared to wildtype controls, (2) analyzed a possible impact of MCP-1 on 
      astrocyte activation (3) investigated the cellular origin of respective 
      inflammatory cytokines and (4) analyzed the impact of MCP-1 secretion on the 
      migration of both neutrophil granulocytes and T-cells. Here we report that 
      MCP-1-deficiency leads to a shift towards a less inflammatory state following 
      experimental occlusion of the middle cerebral artery including an impaired 
      induction of interleukin-6, interleukin-1beta and granulocyte-colony stimulating 
      factor expression as well as a subsequent diminished influx of hematogenous 
      cells. Additionally, MCP-1-deficient mice developed smaller infarcts 36 hours 
      after experimental stroke. Investigations revealed no differences in 
      transcription of tumor necrosis factor-alpha and astrogliosis 12 and 36 hours after 
      onset of ischemia. These novel results help to understand post ischemic, 
      inflammatory mechanisms and might give further arguments towards therapeutical 
      interventions by modulation of MCP-1 expression in post stroke inflammation.
FAU - Strecker, Jan-Kolja
AU  - Strecker JK
AD  - Department of Neurology, University of Munster, Munster, Germany. 
      strecker.jan@gmx.de
FAU - Minnerup, Jens
AU  - Minnerup J
FAU - Gess, Burkhard
AU  - Gess B
FAU - Ringelstein, E Bernd
AU  - Ringelstein EB
FAU - Schabitz, Wolf-Rudiger
AU  - Schabitz WR
FAU - Schilling, Matthias
AU  - Schilling M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111021
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/genetics/*metabolism
MH  - Chemokine CCL2/*deficiency/genetics/*metabolism
MH  - Granulocyte Colony-Stimulating Factor/genetics/*metabolism
MH  - Immunohistochemistry
MH  - Interleukin-1beta/genetics/*metabolism
MH  - Interleukin-6/genetics/*metabolism
MH  - Laser Capture Microdissection
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Real-Time Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
PMC - PMC3198727
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2011/10/28 06:00
MHDA- 2012/05/30 06:00
PMCR- 2011/10/21
CRDT- 2011/10/28 06:00
PHST- 2011/04/13 00:00 [received]
PHST- 2011/09/13 00:00 [accepted]
PHST- 2011/10/28 06:00 [entrez]
PHST- 2011/10/28 06:00 [pubmed]
PHST- 2012/05/30 06:00 [medline]
PHST- 2011/10/21 00:00 [pmc-release]
AID - PONE-D-11-06796 [pii]
AID - 10.1371/journal.pone.0025863 [doi]
PST - ppublish
SO  - PLoS One. 2011;6(10):e25863. doi: 10.1371/journal.pone.0025863. Epub 2011 Oct 21.