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Tenascin‐R and C in multiple sclerosis lesions: relevance to extracellular matrix remodelling
Author(s) -
NJ Gutowski,
Jia Newcombe,
Cuzner Ml
Publication year - 1999
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.1999.00176.x
Subject(s) - tenascin c , pathology , astrogliosis , remyelination , white matter , tenascin , extracellular matrix , multiple sclerosis , lesion , central nervous system , extravasation , biology , medicine , immunology , immunohistochemistry , myelin , microbiology and biotechnology , endocrinology , fibronectin , magnetic resonance imaging , radiology
In the present study the distribution of the inhibitory extracellular molecules tenascin‐R (TN‐R) and tenascin‐ C (TN‐C) was examined by immunocytochemistry during evolution of the multiple sclerosis (MS) lesion, in which astrogliosis is a prominent feature. Sections were cut from five control cases and from 22 blocks containing lesions representing different pathological stages in 18 cases of secondary progressive MS. Widespread expression of TN‐R was found in the normal human central nervous system (CNS), while that of TN‐C was in general restricted to white matter. In acute MS plaques however, there was a similar striking loss of both TN‐R and TN‐C up to the edge of the lesion, where the macrophage density is greatest, extending into the apparently normal white matter. In subacute lesions a TN‐C and/or TN‐R‐immunopositive reactive astrocyte subpopulation was prominent, reflecting synthesis of extracellular matrix molecules. Both tenascins were expressed throughout chronic MS plaques at levels similar to those seen in adjacent white matter. The loss of TN‐R and TN‐C in acute plaques is indicative of enzyme‐mediated breakdown of the matrix which may be a marker of blood–brain barrier breakdown and leucocyte extravasation. Subsequent production of tenascins by reactive astrocytes may result in glial scar formation impeding remyelination and axonal repair in MS lesions.