PMID- 16919250
OWN - NLM
STAT- MEDLINE
DCOM- 20061213
LR  - 20161124
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1113
IP  - 1
DP  - 2006 Oct 3
TI  - Effect of acidosis on IL-8 and MCP-1 during hypoxia and reoxygenation in human 
      NT2-N neurons.
PG  - 64-73
AB  - Inflammation probably plays a significant role in perinatal brain injury. To 
      study the contribution of locally produced cytokines, the effect on cell death of 
      addition of IL-8 and MCP-1 or antibodies to these, and the impact of acidosis, 
      human postmitotic NT2-N neurons were exposed to 3 h of hypoxia and glucose 
      deprivation and reoxygenated for 21 h. After 3 h of hypoxia with neutral medium, 
      IL-8 was significantly increased compared to controls (150 (100-250)% vs. 100 
      (85-115)%, p=0.023). After 21 h of neutral reoxygenation, both IL-8 (380 
      (110-710)% vs. 150 (85-260)%, p=0.041) and monocyte chemoattractant protein-1 
      (MCP-1) (650 (440-2000)% vs. 310 (230-340)%, p=0.007) were significantly 
      increased compared to controls. After 3 h of hypoxia, both IL-8 (p=0.002) and 
      MCP-1 (p=0.008) were significantly lower in cells with acidotic compared with 
      cells with neutral medium. Acidosis during reoxygenation, however, significantly 
      increased IL-8 release, whereas MCP-1 release was diminished. Similar effects of 
      acidosis were seen in normoxic controls. The cells also secreted RANTES and 
      IP-10, but not 8 other cytokines tested. We found no effect on cell death, 
      measured by MTT assay, of addition of IL-8, MCP-1 or antibodies to these. We 
      conclude that human NT2-N neurons release IL-8 and MCP-1 during 21 h of 
      reoxygenation after 3 h of hypoxia. Acidosis led to a differential effect on IL-8 
      and MCP-1, with increased IL-8 and decreased MCP-1, both during reoxygenation and 
      in normoxic controls. IL-8 and MCP-1 had no effect on cell death.
FAU - Froyland, Elisabeth
AU  - Froyland E
AD  - Department of Pediatric Research, Rikshospitalet-Radiumhospitalet Medical Center 
      and University of Oslo, N-0027 Oslo, Norway. elisabeth.froyland@medisin.uio.no
FAU - Pedersen, Elena Didenko
AU  - Pedersen ED
FAU - Kvissel, Anne-Katrine
AU  - Kvissel AK
FAU - Almaas, Runar
AU  - Almaas R
FAU - Pharo, Anne
AU  - Pharo A
FAU - Skalhegg, Bjorn Steen
AU  - Skalhegg BS
FAU - Mollnes, Tom Eirik
AU  - Mollnes TE
FAU - Rootwelt, Terje
AU  - Rootwelt T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060817
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Antibodies)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Interleukin-8)
RN  - 0 (Neurofilament Proteins)
RN  - 0 (Tetrazolium Salts)
RN  - 0 (Thiazoles)
RN  - 108688-71-7 (neurofilament protein H)
RN  - EUY85H477I (thiazolyl blue)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Acidosis/*metabolism
MH  - Antibodies/pharmacology
MH  - Cell Hypoxia/physiology
MH  - Cell Line
MH  - Chemokine CCL2/immunology/*metabolism
MH  - Chemokine CCL5/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Fluorescent Antibody Technique/methods
MH  - Gene Expression Regulation/*drug effects
MH  - Glucose/deficiency
MH  - Humans
MH  - Hypoxia
MH  - Interleukin-8/immunology/*metabolism
MH  - Neurofilament Proteins/metabolism
MH  - Neurons/*physiology
MH  - Oxygen/*administration & dosage
MH  - Statistics, Nonparametric
MH  - Tetrazolium Salts
MH  - Thiazoles
MH  - Time Factors
EDAT- 2006/08/22 09:00
MHDA- 2006/12/14 09:00
CRDT- 2006/08/22 09:00
PHST- 2005/11/28 00:00 [received]
PHST- 2006/07/02 00:00 [revised]
PHST- 2006/07/08 00:00 [accepted]
PHST- 2006/08/22 09:00 [pubmed]
PHST- 2006/12/14 09:00 [medline]
PHST- 2006/08/22 09:00 [entrez]
AID - S0006-8993(06)02124-X [pii]
AID - 10.1016/j.brainres.2006.07.051 [doi]
PST - ppublish
SO  - Brain Res. 2006 Oct 3;1113(1):64-73. doi: 10.1016/j.brainres.2006.07.051. Epub 
      2006 Aug 17.