Upregulation of ADAM-17 expression in active lesions in multiple sclerosis

PLUMB, J., MCQUAID, S., CROSS, A. K., SURR, J., HADDOCK, G., BUNNING, R. A. D. and WOODROOFE, M. N. (2005). Upregulation of ADAM-17 expression in active lesions in multiple sclerosis. Multiple Sclerosis, 12 (4), 375-385.

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Link to published version:: 10.1191/135248506ms1276oa

Abstract

ADAM-17, a disintegrin and metalloproteinase, is the major proteinase responsible for the cleavage of membrane-bound tumour necrosis factor (TNF) as well as being an active sheddase of other cytokines, cytokine receptors, growth factors and adhesion molecules. TNF is a major proinflammatory cytokine that has been identified as having a pathogenic role in inflammatory diseases within the CNS including multiple sclerosis (MS). Here we report the cellular origin and distribution of ADAM- 17 expression within clinically and neuropathologically confirmed MS and normal control white matter, assessed by immunohistochemistry, western blotting and PCR. ADAM-17 expression was associated with the blood vessel endothelium, activated macrophages/microglia and parenchymal astrocytes in MS white matter. Increased levels of ADAM-17 immunoreactivity were displayed in active lesions with evidence of recent myelin breakdown. Further studies into the functional role of ADAM-17 in the pathogenesis of MS and other inflammatory conditions are required.

Item Type: Article
Research Institute, Centre or Group: Biomedical Research Centre
Identification Number: 10.1191/135248506ms1276oa
Depositing User: Ann Betterton
Date Deposited: 22 Feb 2008
Last Modified: 09 Dec 2009 18:23
URI: http://shura.shu.ac.uk/id/eprint/410

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