PMID- 18942743
OWN - NLM
STAT- MEDLINE
DCOM- 20090513
LR  - 20090317
IS  - 1098-1136 (Electronic)
IS  - 0894-1491 (Linking)
VI  - 57
IP  - 6
DP  - 2009 Apr 15
TI  - Monocyte chemoattractant protein-1 (MCP-1) produced via NF-kappaB signaling 
      pathway mediates migration of amoeboid microglia in the periventricular white 
      matter in hypoxic neonatal rats.
PG  - 604-21
LID - 10.1002/glia.20790 [doi]
AB  - Monocyte chemoattractant protein-1 (MCP-1), a member of beta-chemokine subfamily, 
      regulates the migration of microglia, monocytes, and lymphocytes to the 
      inflammatory site in the central nervous system. We sought to determine if 
      amoeboid microglial cells (AMC) produce MCP-1 that may be linked to migration of 
      AMC in the corpus callosum periventricular white matter in hypoxic neonatal rats. 
      A striking feature in 1-day-old rats subjected to hypoxia was a marked increase 
      in cell numbers of AMC and immunoexpression of MCP-1 and its receptor (CCR(2)). 
      By BrdU immunostaining, there was no significant change in the proliferation rate 
      of AMC after hypoxic exposure when compared with the corresponding control rats. 
      When injected intracerebrally into the corpus callosum of 7-day-old postnatal 
      rats, MCP-1 induced the chemotactic migration of AMC to the injection site. In 
      primary microglial cell culture subjected to hypoxia, there was a significant 
      increase in MCP-1 release involving NF-kappaB signaling pathway. In in vitro 
      chemotaxis assay, the medium derived from hypoxia-treated microglial cultures 
      attracted more migratory microglial cells than that from the control microglial 
      culture. The present results suggest that following a hypoxic insult, AMC in the 
      neonatal rats increase MCP-1 production via NF-kappaB signaling pathway. This 
      induces the migration and accumulation of AMC from the neighboring areas to the 
      periventricular white matter (PWM). It is concluded that the preponderance and 
      active migration of AMC, as well as them being the main cellular source of MCP-1, 
      may offer an explanation for the PWM being susceptible to hypoxic damage in 
      neonatal brain.
CI  - (c) 2008 Wiley-Liss, Inc.
FAU - Deng, Y Y
AU  - Deng YY
AD  - Department of Anatomy, Yong Loo Lin School of Medicine, Blk MD10, 4 Medical 
      Drive, National University of Singapore, Singapore.
FAU - Lu, J
AU  - Lu J
FAU - Ling, E A
AU  - Ling EA
FAU - Kaur, C
AU  - Kaur C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Animals, Newborn
MH  - Cell Movement
MH  - Cells, Cultured
MH  - Cerebral Ventricles/physiopathology
MH  - Chemokine CCL2/*metabolism
MH  - Corpus Callosum/*physiopathology
MH  - Gene Expression
MH  - Hypoxia, Brain/*physiopathology
MH  - Microglia/*physiology
MH  - NF-kappa B/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, CCR2/metabolism
MH  - Signal Transduction
EDAT- 2008/10/24 09:00
MHDA- 2009/05/14 09:00
CRDT- 2008/10/24 09:00
PHST- 2008/10/24 09:00 [pubmed]
PHST- 2009/05/14 09:00 [medline]
PHST- 2008/10/24 09:00 [entrez]
AID - 10.1002/glia.20790 [doi]
PST - ppublish
SO  - Glia. 2009 Apr 15;57(6):604-21. doi: 10.1002/glia.20790.