ADAM-17 and TIMP3 protein and mRNA expression in spinal cord white matter of rats with acute experimental autoimmune encephalomyelitis.

Authors: Plumb, J  Cross, AK  Surr, J  Haddock, G  Smith, T  Bunning, RA  Woodroofe, MN 
Citation: Plumb J, etal., J Neuroimmunol. 2005 Jul;164(1-2):1-9.
Pubmed: (View Article at PubMed) PMID:15878627
DOI: Full-text: DOI:10.1016/j.jneuroim.2005.02.021

Tumour necrosis factor (TNF) is a major immunomodulatory and proinflammatory cytokine implicated in the pathogenesis of multiple sclerosis (MS) and the animal model experimental autoimmune encephalomyelitis (EAE). ADAM-17 cleaves membrane-bound TNF into its soluble form. The distribution and level of ADAM-17 expression within spinal cords of Lewis rats with EAE was investigated. ADAM-17 was associated with endothelial cells in the naive and pre-disease spinal cords. In peak disease astrocytic and inflammatory cells expressed ADAM-17. Upregulation of ADAM-17 mRNA expression was coupled with a decrease in mRNA levels of its inhibitor TIMP3 suggesting a role for ADAM-17 in EAE pathogenesis.


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CRRD Object Information
CRRD ID: 1559178
Created: 2006-01-12
Species: All species
Last Modified: 2006-01-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.