Upregulation of ADAM-17 expression in active lesions in multiple sclerosis |
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Authors: | Plumb J McQuaid S Cross A K Surr J Haddock G Bunning R A D Woodroofe M N |
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Affiliation: | Biomedical Research Centre, Sheffield Hallam University, Howard St, Sheffield S1 1WB, UK. j.plumb@shu.ac.uk |
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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. |
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