An international research team has uncovered a mechanism by which the myelin sheath, crucial for signal transmission between cells, could be regenerated. Published in the journal Glia, a team led by Annika Ulc, Simon van Leeuwen and Andreas Faissner (Ruhr-Universität Bochum, Germany) demonstrated the significance of Vav3, a signaling molecule, as a molecular ‘switch’.
“We hope we’ve identified a potential approach for accelerating myelin repair with pharmacological means,” commented Andreas Faissner, Head of the Department of Cell Morphology and Molecular Neurobiology in Bochum.
The myelin sheath is formed of oligodendrocytes and protects axons, the transmission lines of the nervous system. In disease such as multiple sclerosis, the myelin sheath is damaged, inhibiting the nervous system. In the study, Vav3 was discovered to be a regulating factor in the regeneration of damage to the myelin sheath; in cell cultures without Vav3, new myelin formed more slowly. This builds on earlier work to understand the signalling mechanisms of molecular switches of the RhoA type.
“Combined with our understanding of how important the Vav3 exchange factor is, it might be possible in future to control the molecular switches in such a way as to accelerate the regeneration of the myelin sheath,” concluded Faissner.
Sources: Ulc A, Zeug A, Bauch J et al. The guanine nucleotide exchange factor Vav3 modulates oligodendrocyte precursor differentiation and supports remyelination in white matter lesions. Glia. doi.org/10.1002/glia.23548 (ePub)(online ahead-of-print); https://news.rub.de/english/press-releases/2018-11-30-neurobiology-switch-regeneration-nerve-cell-insulation