beta 1-integrin signaling mediates premyelinating oligodendrocyte survival but is not required for CNS myelination and remyelination

• Type: Article in International Scientific Journal
• Date: 2006

Authors

Benninger, Y (Author) Other; Colognato, H (Author) Other; Thurnherr, T (Author) Other; Franklin, RJM (Author) Other; Leone, DP (Author) Other; Atanasoski, S (Author) Other; Nave, KA (Author) Other; ffrench Constant, C (Author) Other; Suter, U (Author) Other; Relvas, OB (Author) Other

Journal

Title: Journal of Neuroscience

Vol. 26

Pages: 7665-7673

ISSN: 0270-6474

Publisher: Society for Neuroscience

Indexing

ISI Web of Knowledge - 74 Citations

Other information

Authenticus ID: P-00G-8X7

DOI: 10.1532/jneurosci.0444-06.2006

Abstract (EN): Previous reports, including transplantation experiments using dominant-negative inhibition of beta 1-integrin signaling in oligodendrocyte progenitor cells, suggested that beta 1-integrin signaling is required for myelination. Here, we test this hypothesis using conditional ablation of the beta 1-integrin gene in oligodendroglial cells during the development of the CNS. This approach allowed us to study oligodendroglial beta 1-integrin signaling in the physiological environment of the CNS, circumventing the potential drawbacks of a dominant-negative approach. We found that beta 1-integrin signaling has a much more limited role than previously expected. Although it was involved in stage-specific oligodendrocyte cell survival, beta 1-integrin signaling was not required for axon ensheathment and myelination per se. We also found that, in the spinal cord, remyelination occurred normally in the absence of beta 1-integrin. We conclude that, although beta 1-integrin may still contribute to other aspects of oligodendrocyte biology, it is not essential for myelination and remyelination in the CNS.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 9