A central role for the ERK-signaling pathway in controlling Schwann cell plasticity and peripheral nerve regeneration in vivo
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...
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| Published in: | Neuron (Cambridge, Mass.) Vol. 73; no. 4; p. 729 |
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| Main Authors: | , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
23.02.2012
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| ISSN: | 1097-4199, 1097-4199 |
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| Abstract | 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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| AbstractList | 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.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. 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. |
| Author | Collins, Melissa J Lloyd, Alison C Ribeiro, Sara Kerai, Ajay P Napoli, Ilaria Parrinello, Simona Rosenberg, Laura H White, Ian J Woodhoo, Ashwin Harrisingh, Marie C Noon, Luke A |
| Author_xml | – sequence: 1 givenname: Ilaria surname: Napoli fullname: Napoli, Ilaria organization: MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, Gower Street, London WC1E 6BT, UK – sequence: 2 givenname: Luke A surname: Noon fullname: Noon, Luke A – sequence: 3 givenname: Sara surname: Ribeiro fullname: Ribeiro, Sara – sequence: 4 givenname: Ajay P surname: Kerai fullname: Kerai, Ajay P – sequence: 5 givenname: Simona surname: Parrinello fullname: Parrinello, Simona – sequence: 6 givenname: Laura H surname: Rosenberg fullname: Rosenberg, Laura H – sequence: 7 givenname: Melissa J surname: Collins fullname: Collins, Melissa J – sequence: 8 givenname: Marie C surname: Harrisingh fullname: Harrisingh, Marie C – sequence: 9 givenname: Ian J surname: White fullname: White, Ian J – sequence: 10 givenname: Ashwin surname: Woodhoo fullname: Woodhoo, Ashwin – sequence: 11 givenname: Alison C surname: Lloyd fullname: Lloyd, Alison C |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22365547$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Animals, Newborn Benzamides - pharmacology Cell Movement - drug effects Cyclin D1 - metabolism Cytokines - metabolism Diphenylamine - analogs & derivatives Diphenylamine - pharmacology Estrogen Antagonists - pharmacology Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Leukocytes - pathology Male MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - genetics MAP Kinase Signaling System - physiology Mast Cells - pathology Mice Mice, Inbred C57BL Mice, Transgenic Microscopy, Confocal Microscopy, Electron, Transmission Microscopy, Immunoelectron Motor Activity - drug effects Motor Activity - genetics Myelin Sheath - genetics Myelin Sheath - metabolism Nerve Regeneration - drug effects Nerve Regeneration - genetics Neutrophils - metabolism Neutrophils - pathology Peripheral Nerve Injuries - pathology Peripheral Nerve Injuries - physiopathology Proto-Oncogene Proteins c-raf - genetics Proto-Oncogene Proteins c-raf - metabolism Reaction Time - drug effects Reaction Time - genetics Receptor, Nerve Growth Factor - genetics Receptor, Nerve Growth Factor - metabolism Receptors, Estrogen - genetics Recovery of Function - drug effects Recovery of Function - genetics Schwann Cells - physiology Schwann Cells - ultrastructure T-Lymphocytes - metabolism T-Lymphocytes - pathology Tamoxifen - pharmacology Time Factors |
| Title | A central role for the ERK-signaling pathway in controlling Schwann cell plasticity and peripheral nerve regeneration in vivo |
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| Volume | 73 |
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