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</script>Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment
pmid: 19324423
Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment
ADAM-17 expression is localised to endothelial cells in the human central nervous system (CNS) and is increased in multiple sclerosis (MS) white matter, suggesting a role in MS pathogenesis. Expression of ADAM-17, TIMP-3, and fractalkine were investigated in a human brain endothelial cell line (hCMEC/D3) after pro-inflammatory cytokine treatment. Tumour necrosis factor (TNF) significantly increased fractalkine mRNA (>100 fold) and protein expression, which was associated with increased shedding of fractalkine from the cell. Fractalkine shedding may regulate immune cell trafficking into the CNS, however, this does not appear to be directly controlled by ADAM-17 activity.
- University of Paris France
- French National Centre for Scientific Research France
- Cornell University United States
- Sheffield Teaching Hospitals NHS Foundation Trust United Kingdom
- Royal Hallamshire Hospital United Kingdom
Tissue Inhibitor of Metalloproteinase-3, Chemokine CX3CL1, Tumor Necrosis Factor-alpha, Endothelial Cells, Gene Expression, ADAM17 Protein, Cell Line, Up-Regulation, ADAM Proteins, Chemotaxis, Leukocyte, Cytokines, Encephalitis, Humans, RNA, Messenger
Tissue Inhibitor of Metalloproteinase-3, Chemokine CX3CL1, Tumor Necrosis Factor-alpha, Endothelial Cells, Gene Expression, ADAM17 Protein, Cell Line, Up-Regulation, ADAM Proteins, Chemotaxis, Leukocyte, Cytokines, Encephalitis, Humans, RNA, Messenger
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