PMID- 15689362
OWN - NLM
STAT- MEDLINE
DCOM- 20050420
LR  - 20220310
IS  - 1460-2156 (Electronic)
IS  - 0006-8950 (Linking)
VI  - 128
IP  - Pt 4
DP  - 2005 Apr
TI  - Involvement of monocyte chemoattractant protein-1, macrophage inflammatory 
      protein-1alpha and interleukin-1beta in Wallerian degeneration.
PG  - 854-66
AB  - Wallerian degeneration in the CNS and PNS consists of degradation and 
      phagocytosis of axons and their myelin sheath distal to the site of injury. This 
      process of degeneration, which requires an effective macrophage response, occurs 
      rapidly in peripheral nerves but is slow in the CNS. Rapid Wallerian degeneration 
      in peripheral nerves may contribute to subsequent axonal regeneration. We show 
      that there is a marked increase in mRNA expression of three pro-inflammatory 
      molecules, the chemokines monocyte chemoattractant protein-1 (MCP-1) and 
      macrophage inflammatory protein-1alpha (MIP-1alpha), and the cytokine 
      interleukin-1beta (IL-1beta), in the mouse sciatic nerve but not in the spinal 
      cord undergoing Wallerian degeneration. Neutralizing MCP-1, MIP-1alpha and 
      IL-1beta in the lesioned sciatic nerve with function-blocking antibodies 
      suppressed macrophage responses and myelin clearance. Injecting recombinant 
      MCP-1, MIP-1alpha or IL-1beta into the normal, uninjured spinal cord triggered 
      the expression of a number of chemokines and cytokines. Furthermore, injecting 
      recombinant MCP-1/MIP-1alpha or IL-1beta into the dorsal column of the spinal 
      cord undergoing Wallerian degeneration triggered rapid macrophage/microglial 
      activation and myelin clearance. These findings provide direct evidence that 
      MCP-1, MIP-1alpha and IL-1beta are important regulators of macrophage responses 
      that lead to rapid myelin breakdown and clearance in Wallerian degeneration.
FAU - Perrin, Florence E
AU  - Perrin FE
AD  - Centre for Research in Neuroscience, McGill University Health Center, Montreal, 
      Quebec, Canada.
FAU - Lacroix, Steve
AU  - Lacroix S
FAU - Aviles-Trigueros, Marcelino
AU  - Aviles-Trigueros M
FAU - David, Samuel
AU  - David S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050202
PL  - England
TA  - Brain
JT  - Brain : a journal of neurology
JID - 0372537
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/physiology
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Cytokines/genetics/*physiology
MH  - Female
MH  - Gene Expression
MH  - Interleukin-1/physiology
MH  - Macrophage Activation/drug effects
MH  - Macrophage Inflammatory Proteins/physiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Microinjections
MH  - Microscopy, Electron
MH  - Myelin Sheath/metabolism
MH  - Phagocytosis/drug effects
MH  - RNA, Messenger/genetics
MH  - Recombinant Proteins/pharmacology
MH  - Sciatic Nerve/immunology/injuries/ultrastructure
MH  - Spinal Cord Injuries/complications/*metabolism/pathology
MH  - Wallerian Degeneration/etiology/*metabolism/pathology
EDAT- 2005/02/04 09:00
MHDA- 2005/04/21 09:00
CRDT- 2005/02/04 09:00
PHST- 2005/02/04 09:00 [pubmed]
PHST- 2005/04/21 09:00 [medline]
PHST- 2005/02/04 09:00 [entrez]
AID - awh407 [pii]
AID - 10.1093/brain/awh407 [doi]
PST - ppublish
SO  - Brain. 2005 Apr;128(Pt 4):854-66. doi: 10.1093/brain/awh407. Epub 2005 Feb 2.