PMID- 12111830
OWN - NLM
STAT- MEDLINE
DCOM- 20020814
LR  - 20071115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 68
IP  - 6
DP  - 2002 Jun 15
TI  - Monocyte recruitment and myelin removal are delayed following spinal cord injury 
      in mice with CCR2 chemokine receptor deletion.
PG  - 691-702
AB  - The inflammatory response initiated after spinal cord injury (SCI) is 
      characterized by the accumulation of macrophages at the impact site. Monocyte 
      chemoattractant protein-1 (MCP-1) is a strong candidate for mediating chemotaxis 
      of monocytes to the injured nervous system. To help in defining the role of MCP-1 
      in inflammation after SCI, we evaluated the time course of macrophage 
      accumulation for 2 weeks following a midthoracic spinal cord contusion injury in 
      mice lacking CCR2, a principal receptor for MCP-1. Mice with a deletion of CCR2 
      resulted in significantly reduced Mac-1 immunoreactivity restricted to the lesion 
      epicenter at 7 days postinjury. The regions devoid of Mac-1 immunoreactivity 
      corresponded to areas of reduced myelin degradation at this time. By 14 days 
      postinjury, however, there were no differences in Mac-1 staining between CCR2 
      (+/+) and CCR2 (-/-) mice. Analyses of mRNA levels by RNase protection assay 
      (RPA) revealed increases in MCP-1 as well as MCP-3 and MIP-2 mRNA at 1 day 
      postinjury compared with 7 day postinjury. There were no differences in chemokine 
      expression between CCR2-deficient mice and wild-type littermate controls. The 
      CCR2-deficient mice also exhibited reduced expression of mRNA for chemokine 
      receptors CCR1 and CCR5. Together, these results indicate that chemokines acting 
      through CCR2 contribute to the early recruitment of monocytes to the lesion 
      epicenter following SCI.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Ma, Manhong
AU  - Ma M
AD  - Department of Physiology and Cell Biology, College of Medicine and Public Health, 
      The Ohio State University, Columbus, Ohio, USA.
FAU - Wei, Tao
AU  - Wei T
FAU - Boring, Landin
AU  - Boring L
FAU - Charo, Israel F
AU  - Charo IF
FAU - Ransohoff, Richard M
AU  - Ransohoff RM
FAU - Jakeman, Lyn B
AU  - Jakeman LB
LA  - eng
GR  - HL52773/HL/NHLBI NIH HHS/United States
GR  - NS32151/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Monocyte Chemoattractant Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/metabolism
MH  - Contusions
MH  - Immunohistochemistry
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Monocyte Chemoattractant Proteins/*metabolism
MH  - *Monocytes/metabolism
MH  - Myelin Sheath/*metabolism
MH  - *Phagocytosis
MH  - RNA, Messenger/genetics
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/*genetics
MH  - Spinal Cord Injuries/*metabolism
MH  - Time Factors
EDAT- 2002/07/12 10:00
MHDA- 2002/08/15 10:01
CRDT- 2002/07/12 10:00
PHST- 2002/07/12 10:00 [pubmed]
PHST- 2002/08/15 10:01 [medline]
PHST- 2002/07/12 10:00 [entrez]
AID - 10.1002/jnr.10269 [doi]
PST - ppublish
SO  - J Neurosci Res. 2002 Jun 15;68(6):691-702. doi: 10.1002/jnr.10269.