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Journal Article

A role for Schwann cell-derived neuregulin-1 in remyelination

MPS-Authors
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Stassart,  Ruth M.
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Fledrich,  Robert
Molecular and translational neurology, Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Velanac,  Viktorija
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Brinkmann,  Bastian G.
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Schwab,  Markus H.
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Sereda,  Michael W.
Molecular and translational neurology, Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182320

Nave,  Klaus-Armin
Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Citation

Stassart, R. M., Fledrich, R., Velanac, V., Brinkmann, B. G., Schwab, M. H., Meijer, D., et al. (2013). A role for Schwann cell-derived neuregulin-1 in remyelination. Nature Neuroscience, 16(1), 48-54. doi:10.1038/nn.3281.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002A-52E5-F
Abstract
After peripheral nerve injury, axons regenerate and become remyelinated by resident Schwann cells. However, myelin repair never results in the original myelin thickness, suggesting insufficient stimulation by neuronal growth factors. Upon testing this hypothesis, we found that axonal neuregulin-1 (NRG1) type III and, unexpectedly, also NRG1 type I restored normal myelination when overexpressed in transgenic mice. This led to the observation that Wallerian degeneration induced de novo NRG1 type I expression in Schwann cells themselves. Mutant mice lacking a functional Nrg1 gene in Schwann cells are fully myelinated but exhibit impaired remyelination in adult life. We suggest a model in which loss of axonal contact triggers denervated Schwann cells to transiently express NRG1 as an autocrine/paracrine signal that promotes Schwann cell differentiation and remyelination.