Journal
NEURON
Volume 73, Issue 4, Pages 729-742Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2011.11.031
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Funding
- AICR
- CRUK
- Wellcome Trust
- EMBO
- Cancer Research UK [11244] Funding Source: researchfish
- Worldwide Cancer Research [12-0041] Funding Source: researchfish
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Following damage to peripheral nerves, a remarkable process of clearance and regeneration takes place. Axons downstream of the injury degenerate, while the nerve is remodeled to direct axonal regrowth. Schwann cells are important for this regenerative process. Sensing damaged axons, they dedifferentiate to a progenitor-like state, in which they aid nerve regeneration. Here, we demonstrate that activation of an inducible Raf-kinase transgene in myelinated Schwann cells is sufficient to control this plasticity by inducing severe demyelination in the absence of axonal damage, with the period of demyelination/ataxia determined by the duration of Raf activation. Remarkably, activation of Raf-kinase also induces much of the inflammatory response important for nerve repair, including breakdown of the blood-nerve barrier and the influx of inflammatory cells. This reversible in vivo model identifies a central role for ERK signaling in Schwann cells in orchestrating nerve repair and is a powerful system for studying peripheral neuropathies and cancer.
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