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Updated: May 14, 2026
08:57
Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
Published on: March 26, 2015
Fibronectin aggregation in multiple sclerosis lesions impairs remyelination
Josephine M J Stoffels1, Jenny C de Jonge, Mirjana Stancic
1Department of Cell Biology, University Medical Centre Groningen, University of Groningen, A. Deusinglaan 1, 9713 AV Groningen, The Netherlands.
Brain : a Journal of Neurology
|February 1, 2013
Summary
Fibronectin aggregates in multiple sclerosis lesions inhibit remyelination by blocking oligodendrocyte progenitor differentiation. Targeting these aggregates may promote repair in demyelinating diseases.
Area of Science:
- Neuroscience
- Cell Biology
- Extracellular Matrix Biology
Background:
- Remyelination is crucial for preventing axon degeneration after central nervous system demyelination.
- Remyelination failure in diseases like multiple sclerosis is linked to extracellular signaling changes.
- The role of fibronectin in remyelination failure requires further investigation.
Purpose of the Study:
- To investigate fibronectin expression during demyelinating injury.
- To determine the impact of fibronectin on oligodendrocyte progenitor remyelination.
- To explore fibronectin aggregation in multiple sclerosis and its potential role in disease pathogenesis.
Main Methods:
- Analyzing fibronectin expression in toxin-induced and experimental autoimmune encephalitis models.
- Investigating fibronectin production by central nervous system cells.
- Assessing the effect of astrocyte-derived fibronectin aggregates on oligodendrocyte differentiation and remyelination in vivo.
Main Results:
- Transient fibronectin increase during efficient remyelination, followed by decline.
- Persistent fibronectin aggregates in chronic multiple sclerosis lesions and during experimental autoimmune encephalitis relapse.
- Inflammation-induced fibronectin aggregation by astrocytes.
- Astrocyte-derived fibronectin aggregates inhibited oligodendrocyte differentiation and remyelination.
Conclusions:
- Fibronectin aggregates in multiple sclerosis lesions contribute to remyelination failure.
- Fibronectin aggregation is associated with inflammation-induced demyelination.
- Therapeutic strategies targeting fibronectin aggregates could promote remyelination.
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