PMID- 9270493
OWN - NLM
STAT- MEDLINE
DCOM- 19970918
LR  - 20161124
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 17
IP  - 7
DP  - 1997 Jul
TI  - Hypoxic-ischemic injury induces monocyte chemoattractant protein-1 expression in 
      neonatal rat brain.
PG  - 759-70
AB  - Monocyte chemoattractant protein-1 (MCP-1) regulates monocyte accumulation in 
      several macrophage-dependent experimental disease models. In the neonatal brain, 
      activated microglia accumulate rapidly after hypoxic-ischemic injury. These cells 
      produce potentially neurotoxic factors that may contribute to the progression of 
      injury. To determine whether MCP-1 could be one of the molecular signals that 
      influences the microglial response to hypoxic-ischemic injury in the neonatal 
      brain, we examined the impact of acute hypoxic-ischemic injury on MCP-1 mRNA and 
      protein expression. Seven-day-old rats underwent right carotid artery ligation, 
      followed by 3 hours of 8% oxygen exposure, to elicit ipsilateral forebrain 
      hypoxic-ischemic injury. To detect MCP-1 mRNA in situ hybridization assays were 
      performed using 35S-labeled antisense riboprobes generated from rat MCP-1 cDNA. 
      Animals were evaluated 0, 1, 2, 4, 8, 16, 24, 48, and 120 hours after hypoxic 
      exposure (N > or = 3/group). Immunocytochemistry (with a polyclonal rabbit 
      antirat MCP-1 antibody) was used to determine the anatomic and temporal 
      distribution of MCP-1, in samples obtained 10 minutes to 5 days after hypoxic 
      exposure (N > or = 3/group). Monocyte chemoattractant protein-1 mRNA was first 
      detected in periventricular regions of the lesioned hemisphere 1 hour after 
      hypoxia-ischemia; periependymal and intraparenchymal MCP-1 mRNA expression were 
      detected at 4 hours; hybridization signal peaked at 8 to 24 hours; and no MCP-1 
      mRNA was detected at 48 and 120 hours. In lesioned forebrain, MCP-1 protein 
      expression were consistently detected at 2.5 to 48 hours after hypoxia-ischemia. 
      Many immunoreactive cells appeared to be neurons. These results suggest that in 
      the developing brain, MCP-1 could represent a functionally important molecular 
      signal for the microglial response to hypoxic-ischemic injury.
FAU - Ivacko, J
AU  - Ivacko J
AD  - Department of Pediatrics, University of Michigan, Ann Arbor 48109-0646, USA.
FAU - Szaflarski, J
AU  - Szaflarski J
FAU - Malinak, C
AU  - Malinak C
FAU - Flory, C
AU  - Flory C
FAU - Warren, J S
AU  - Warren JS
FAU - Silverstein, F S
AU  - Silverstein FS
LA  - eng
GR  - HL 48287/HL/NHLBI NIH HHS/United States
GR  - NS 31054/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
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  - Animals, Newborn/*metabolism
MH  - Brain/*metabolism
MH  - Brain Ischemia/*metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Hypoxia/*metabolism
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
AID - 10.1097/00004647-199707000-00006 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 1997 Jul;17(7):759-70. doi: 
      10.1097/00004647-199707000-00006.