The collapsin response mediator protein 5 onconeural protein is expressed in Schwann cells under axonal signals and regulates axon-Schwann cell interactions
Autor: | Jean-Philippe Camdessanché, Karine Ferraud, Monique Touret, Nadia Boutahar, François Lassabliere, Pappachan E. Kolattukudy, Jean-Christophe Antoine, Marie Mutter, Jérôme Honnorat |
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Rok vydání: | 2012 |
Předmět: |
Hydrolases
Cell Schwann cell Nerve Tissue Proteins Cell Communication Biology Pathology and Forensic Medicine Amidohydrolases Cellular and Molecular Neuroscience Myelin chemistry.chemical_compound Mice medicine Animals Humans Cyclic adenosine monophosphate Axon Cells Cultured Mice Knockout Regeneration (biology) General Medicine Axons Coculture Techniques Rats medicine.anatomical_structure nervous system Neurology chemistry Animals Newborn Gene Expression Regulation Neuregulin Neurology (clinical) Sciatic nerve Schwann Cells Neuroscience Microtubule-Associated Proteins Signal Transduction |
Zdroj: | Journal of neuropathology and experimental neurology. 71(4) |
ISSN: | 1554-6578 |
Popis: | Collapsin response mediator protein 5 (CRMP5) is one of the rare peripheral nerve antigens that is a target of autoantibodies in a paraneoplastic peripheral neuropathy. The pattern of axonal and myelin alterations suggests that CRMP5 is involved in axon-Schwann cell interaction. We examined CRMP5 expression and function in primary cultures of Schwann cells and neurons and at various developmental and regenerating stages of rat sciatic nerve and in CRMP5 -deficient mice in vivo. Collapsin response mediator protein 5 was strongly expressed during postnatal development and regeneration and decreased with myelination. It was mainly expressed by immature Schwann cells and persisted in Remak cells in the adult; however, a subpopulation of Schwann cells that were induced to myelinate also expressed CRMP5 . We identified 2 axonal molecular cues regulating CRMP5 expression: human neuregulin type 1, which induces CRMP5 expression in immature and premyelinating Schwann cells, and cyclic adenosine monophosphate, which inhibits CRMP5 expression when Schwann cells begin myelination. Collapsin response mediator protein 5-deficient mice showed abnormal Schwann process extension resulting in abnormal cell-axon segregation, indicating that CRMP5 is involved in the morphologic adaptation of Schwann cells to surround axons. These results demonstrate the importance of CRMP5 in axonYSchwann cell cooperation during development and regeneration. |
Databáze: | OpenAIRE |
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