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Hochmeister, S; Romauch, M; Bauer, J; Seifert-Held, T; Weissert, R; Linington, C; Hartung, HP; Fazekas, F; Storch, MK.
Re-expression of N-Cadherin in remyelinating lesions of experimental inflammatory demyelination.
Exp Neurol. 2012; 237(1):70-77
Doi: 10.1016/j.expneurol.2012.06.010
Web of Science
PubMed
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FullText_MUG
- Leading authors Med Uni Graz
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Hochmeister Sonja
- Co-authors Med Uni Graz
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Fazekas Franz
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Romauch Matthias
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Seifert-Held Thomas
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Storch Maria
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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 downregulated 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.
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Animals -
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Cadherins - biosynthesis
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Encephalomyelitis, Autoimmune, Experimental - genetics
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Female -
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Inflammation - genetics
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Myelin Proteins - biosynthesis
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Myelin Sheath - physiology
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Myelin-Oligodendrocyte Glycoprotein -
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Rats -
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Time Factors -
- Find related publications in this database (Keywords)
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N-cadherin
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Experimental autoimmune encephalomyelitis
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Multiple sclerosis
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Myelin oligodendrocyte glycoprotein
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Remyelination