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First published online September 20, 2006

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Nerve regeneration Schwannns along

Loss of nerve axons and defective axonal regeneration cause permanent disability in people with peripheral neuropathy. Normal axonal regeneration in the peripheral nervous system involves interactions between Schwann cells, the extracellular matrix and regrowing axons. These poorly understood interactions involve cell-surface receptors and cytoskeletal molecules. On p. 3981, Stefano Previtali and colleagues reveal an important role for the intermediate filament protein glial fibrillary acidic protein (GFAP) in axonal regeneration after nerve injury. They show that peripheral nerve development is normal in GFAP-null mice, probably because vimentin (another intermediate filament protein) and other cytoskeletal components compensate for the absence of GFAP. However, axonal regeneration is delayed after injury, probably because Schwann cell proliferation, which is crucial for successful regeneration, is defective. They also show that GFAP binds integrin vß8 to initiate mitotic signals soon after damage whereas vimentin binds integrin 5ß1 to regulate Schwann cell proliferation later in regeneration. Since nerve repair is partly abolished in GFAP mutants, the authors conclude that defective GFAP function might be involved in some peripheral neuropathies.

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Loss of glial fibrillary acidic protein (GFAP) impairs Schwann cell proliferation and delays nerve regeneration after damage

Daniela Triolo, Giorgia Dina, Isabella Lorenzetti, MariaChiara Malaguti, Paolo Morana, Ubaldo Del Carro, Giancarlo Comi, Albee Messing, Angelo Quattrini, and Stefano C. Previtali
JCS 2006 119: 3981-3993. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?