PMID- 11891436
OWN - NLM
STAT- MEDLINE
DCOM- 20020502
LR  - 20071115
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 22
IP  - 3
DP  - 2002 Mar
TI  - Monocyte chemoattractant protein-1 deficiency is protective in a murine stroke 
      model.
PG  - 308-17
AB  - Inflammatory processes have been implicated in the pathogenesis of brain damage 
      after stroke. In rodent stroke models, focal ischemia induces several 
      proinflammatory chemokines, including monocyte chemoattractant protein-1 (MCP-1). 
      The individual contribution to ischemic tissue damage, however, is largely 
      unknown. To address this question, the authors subjected MCP-1-deficient mice 
      (MCP-1-/-) to permanent middle cerebral artery occlusion (MCAO). Measurement of 
      basal blood pressure, cerebral blood flow, and blood volume revealed no 
      differences between wild-type (wt) and MCP-1-/- mice. MCAO led to similar 
      cerebral perfusion deficits in wt and MCP-1-/- mice, excluding differences in the 
      MCA supply territory and collaterals. However, compared with wt mice, the mean 
      infarct volume was 29% smaller in MCP-1-/- mice 24 hours after MCAO (P = 0.022). 
      Immunostaining showed a reduction of phagocytic macrophage accumulation within 
      infarcts and the infarct border in MCP-1-/- mice 2 weeks after MCAO. At the same 
      time point, the authors found an attenuation of astrocytic hypertrophy in the 
      infarct border and thalamus in MCP-1-/- mice. However, these effects on 
      macrophages and astrocytes in MCP-1-/- mice occurred too late to suggest a 
      protective role in acute infarct growth. Of note: at 6 hours after MCAO, MCP-1-/- 
      mice produced significantly less interleukin-1beta in ischemic tissue; this might 
      be related to tissue protection. The results of this study indicate that 
      inhibition of MCP-1 signaling could be a new acute treatment approach to limit 
      infarct size after stroke.
FAU - Hughes, Paula M
AU  - Hughes PM
AD  - Nervous System Research, Core Technology Area, Novartis Pharma AG, Basel, 
      Switzerland.
FAU - Allegrini, Peter R
AU  - Allegrini PR
FAU - Rudin, Markus
AU  - Rudin M
FAU - Perry, V Hugh
AU  - Perry VH
FAU - Mir, Anis K
AU  - Mir AK
FAU - Wiessner, Christoph
AU  - Wiessner C
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Blood Pressure
MH  - Cerebral Infarction/*pathology
MH  - Cerebrovascular Circulation/*physiology
MH  - Chemokine CCL2/*deficiency/genetics/physiology
MH  - Crosses, Genetic
MH  - Magnetic Resonance Imaging
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Middle Cerebral Artery
MH  - Reference Values
MH  - Stroke/pathology/*prevention & control
MH  - Thalamus/pathology
EDAT- 2002/03/14 10:00
MHDA- 2002/05/03 10:01
CRDT- 2002/03/14 10:00
PHST- 2002/03/14 10:00 [pubmed]
PHST- 2002/05/03 10:01 [medline]
PHST- 2002/03/14 10:00 [entrez]
AID - 10.1097/00004647-200203000-00008 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2002 Mar;22(3):308-17. doi: 
      10.1097/00004647-200203000-00008.