Re-expression of N-cadherin in remyelinating lesions of experimental inflammatory demyelination

Hochmeister, S. and Romauch, M. and Bauer, J. and Seifert-Held, T. and Weissert, R. and Linington, C. and Hartung, H. P. and Fazekas, F. and Storch, M. K. (2012) Re-expression of N-cadherin in remyelinating lesions of experimental inflammatory demyelination. EXPERIMENTAL NEUROLOGY, 237 (1). pp. 70-77. ISSN 0014-4886, 1090-2430

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Abstract

The cell adhesion molecule N-cadherin is involved in several processes during central nervous system development, but also in certain pathologic conditions in the adult brain, including tumorigenesis and Alzheimer's disease. N-cadherin function in inflammatory demyelinating disease has so far not been investigated. In vitro studies suggest a role of N-cadherin in myelination; on the other hand N-cadherin has been implicated in the formation of the glial scar, which is believed to impede remyelination. The aim of our study was to investigate the expression pattern of N-cadherin immunoreactivity in experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein (MOG-EAE), an animal model closely mimicking multiple sclerosis. It allows a detailed evaluation of all stages of de- and remyelination during lesion development. Immunopathological evaluation was performed on paraffin-embedded CNS sections sampled at days 20 to 120 post immunization. We found a predominant expression of N-cadherin on oligodendrocytes in early remyelinating lesions, while in fully remyelinated shadow plaques there was no detectable immunoreactivity for N-cadherin. This expression pattern indicates a role of N-cadherin in the initiation of remyelination, most likely by providing a guidance between myelin lamellae and oligodendrocytes. Once the initial contact is made N-cadherin is then rapidly down-regulated and virtually absent after completion of the repair process, analog to its known role in developmental myelination. Our results show that N-cadherin plays an important role in creating a remyelination-facilitating environment. (C) 2012 Elsevier Inc. All rights reserved.

Item Type: Article
Uncontrolled Keywords: CELL-CELL ADHESION; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN-OLIGODENDROCYTE-GLYCOPROTEIN; MULTIPLE-SCLEROSIS PATHOLOGY; DIFFERENTIAL EXPRESSION; AXONAL-INJURY; MOUSE-BRAIN; GLIAL SCAR; RAT; MOLECULE; N-cadherin; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Myelin oligodendrocyte glycoprotein; Remyelination
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Neurologie
Depositing User: Dr. Gernot Deinzer
Date Deposited: 07 May 2020 05:08
Last Modified: 07 May 2020 05:08
URI: https://pred.uni-regensburg.de/id/eprint/18245

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