Neuropathol Appl Neurobiol 2002 Apr;28(2):168-9
Holley JE, Gveric D, Newcombe J, Gutowski NJ.
Centre for Cell & Molecular Biology (Neurology), University of Exeter, Exeter, UK
Experimental Neuroinflammation Group, Institute of Neurology, UCL, London, UK
Dense astrocytic scarring in chronic multiple sclerosis (MS) plaques inhibits tissue repair. However, at the rim of a lesion the glial scar fails to form despite the presence of reactive astrocytes. Animal studies have shown that astrocyte antigen expression varies depending on astrocyte type and location. Characterization of human astrocytes in MS tissue may identify markers relevant to the glial scar.
MATERIALS AND METHODS:
Astrocyte antigenic phenotype was investigated in subventricular white matter by immunocytochemistry and Western blotting. Snap-frozen tissue from normal controls (n = 4), MS normal appearing white matter (n = 5) and lesions [acute (n = 7), subacute (n = 7) and chronic (n = 13)] was studied.
As expected, glial fibrillary acidic protein and vimentin expression was elevated in scar astrocytes. In addition there was increased expression of nestin, embryonic neural cell adhesion molecule, epidermal growth factor receptor, nerve growth factor and its receptor p75, and in a subpopulation of scar astrocytes, basic fibroblast growth factor.
Changes in expression of proteins associated with development, growth factors and growth factor receptors are characteristic of the scar astrocyte phenotype in chronic MS lesions. These proteins may be of relevance to glial scar formation and tissue repair.