PMID- 20068578
OWN - NLM
STAT- MEDLINE
DCOM- 20100617
LR  - 20211020
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 30
IP  - 6
DP  - 2010 Jun
TI  - The interaction between tumor necrosis factor-like weak inducer of apoptosis and 
      its receptor fibroblast growth factor-inducible 14 promotes the recruitment of 
      neutrophils into the ischemic brain.
PG  - 1147-56
LID - 10.1038/jcbfm.2009.280 [doi]
AB  - Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor 
      fibroblast growth factor-inducible 14 (Fn14) are expressed in endothelial cells 
      and perivascular astrocytes. Here, we show that TWEAK induces a dose-dependent 
      increase in the expression of the chemokine monocyte chemoattractant protein-1 
      (MCP-1) in astrocytes, and that this effect is mediated by its interaction with 
      Fn14 via nuclear factor-kappaB pathway activation. Exposure to oxygen-glucose 
      deprivation (OGD) conditions increases TWEAK and Fn14 mRNA expression in 
      wild-type (Wt) astrocytic cultures. Likewise, incubation under OGD conditions 
      induces the expression of MCP-1 in Wt astrocytes but not in astrocytes deficient 
      on either TWEAK (TWEAK(-/-)) or Fn14 (Fn14(-/-)). We also found that TWEAK 
      induces the passage of neutrophils to the abluminal side of an in vitro model of 
      the blood-brain barrier. Our earlier studies indicate that cerebral ischemia 
      increases the expression of TWEAK and Fn14 in the endothelial cell-basement 
      membrane-astrocyte interface. Here, we report that middle cerebral artery 
      occlusion increases the expression of MCP-1 and the recruitment of neutrophils 
      into the ischemic tissue in Wt but not in TWEAK(-/-) or Fn14(-/-) mice. These 
      novel results indicate that during cerebral ischemia, the interaction between 
      TWEAK and Fn14 leads to the recruitment of leukocytes into the ischemic tissue.
FAU - Haile, Woldeab B
AU  - Haile WB
AD  - Department of Neurology, Center for Neurodegenerative Disease, Emory University 
      School of Medicine, Atlanta, Georgia 30322, USA.
FAU - Echeverry, Ramiro
AU  - Echeverry R
FAU - Wu, Jialing
AU  - Wu J
FAU - Yepes, Manuel
AU  - Yepes M
LA  - eng
GR  - R01 NS062073/NS/NINDS NIH HHS/United States
GR  - R56 HL095063/HL/NHLBI NIH HHS/United States
GR  - NS-062073/NS/NINDS NIH HHS/United States
GR  - HL-095063/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20100113
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 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokine TWEAK)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (TNFRSF12A protein, human)
RN  - 0 (TWEAK Receptor)
RN  - 0 (Tnfrsf12a protein, mouse)
RN  - 0 (Tnfsf12 protein, mouse)
RN  - 0 (Tumor Necrosis Factors)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism/pathology
MH  - Brain Ischemia/genetics/*metabolism/pathology
MH  - Cell Hypoxia
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Cytokine TWEAK
MH  - Endothelial Cells/*metabolism/pathology
MH  - Gene Expression Regulation/genetics
MH  - Glucose/metabolism
MH  - Humans
MH  - Mice
MH  - Mice, Knockout
MH  - *Neutrophil Infiltration
MH  - Neutrophils/*metabolism/pathology
MH  - Receptors, Tumor Necrosis Factor/genetics/*metabolism
MH  - TWEAK Receptor
MH  - Tumor Necrosis Factors/genetics/*metabolism
PMC - PMC2949208
EDAT- 2010/01/14 06:00
MHDA- 2010/06/18 06:00
PMCR- 2011/06/01
CRDT- 2010/01/14 06:00
PHST- 2010/01/14 06:00 [entrez]
PHST- 2010/01/14 06:00 [pubmed]
PHST- 2010/06/18 06:00 [medline]
PHST- 2011/06/01 00:00 [pmc-release]
AID - jcbfm2009280 [pii]
AID - 10.1038/jcbfm.2009.280 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2010 Jun;30(6):1147-56. doi: 10.1038/jcbfm.2009.280. 
      Epub 2010 Jan 13.