Abstract
Damage to axons in acute multiple sclerosis (MS) lesions is now well established but the mechanisms of this damage remain obscure. Here we have applied a panel of antibodies that identify cell populations and proteins contained in them with a view to detecting those cells and proteins that are localised particularly closely to damaged axons in acute, sub-acute and border-active MS plaques. Results are expressed semi-quantitatively and graphs produced that show that many of the markers show enhanced expression at sites of axon damage. However, the sharpest increase in expression in relation to axon damage was seen for Calpain I (micro-calpain), inducible nitric oxide synthase and MMP-2, suggesting that these proteins may form part of a group of proteins responsible for the initiation of myelin and/or axon damage seen in MS lesions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / metabolism
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Antigens, CD / biosynthesis
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Antigens, Differentiation, Myelomonocytic / biosynthesis
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Axons / pathology*
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Biomarkers / analysis
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Brain / metabolism
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Brain / pathology*
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CD3 Complex / biosynthesis
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Calpain / biosynthesis
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Humans
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Immunohistochemistry
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Matrix Metalloproteinase 2 / biosynthesis
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Matrix Metalloproteinase 9 / biosynthesis
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Multiple Sclerosis / metabolism
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Multiple Sclerosis / pathology*
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Nitric Oxide Synthase Type II / biosynthesis
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Osteopontin
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Plaque, Amyloid / metabolism*
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Plaque, Amyloid / pathology
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Proteins / metabolism*
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Sialoglycoproteins / biosynthesis
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T-Lymphocytes / metabolism
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Tyrosine / analogs & derivatives
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Tyrosine / biosynthesis
Substances
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Amyloid beta-Peptides
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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Biomarkers
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CD3 Complex
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CD68 antigen, human
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Proteins
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SPP1 protein, human
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Sialoglycoproteins
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Osteopontin
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3-nitrotyrosine
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Tyrosine
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Nitric Oxide Synthase Type II
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Calpain
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Matrix Metalloproteinase 2
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Matrix Metalloproteinase 9