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The Journal of Neuroscience, October 29, 2008, 28(44):11292-11303; doi:10.1523/JNEUROSCI.3068-08.2008

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Development/Plasticity/Repair
Conditional Deletion of the Itgb4 Integrin Gene in Schwann Cells Leads to Delayed Peripheral Nerve Regeneration

Catharina E. E. M. Van der Zee,^1 * Maaike Kreft,^2 * Gaby Beckers,¹ Arthur Kuipers,¹ and Arnoud Sonnenberg²

¹Department of Cell Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Medical Center Nijmegen, 6525 GA Nijmegen, The Netherlands, and ²Division of Cell Biology, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands

Correspondence should be addressed to either of the following: Dr. Catharina E. E. M. Van der Zee, Department of Cell Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Medical Center Nijmegen, Geert Groote plein 28, 6525 GA Nijmegen, The Netherlands, Email: i.vanderzee{at}ncmls.ru.nl; or Dr. Arnoud Sonnenberg, Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands, E-mail: Email: a.sonnenberg{at}nki.nl

Several different integrins participate in the complex interactions that promote repair of the peripheral nervous system. The role of the integrin 6β4 in peripheral nerve regeneration was investigated in mice by cre-mediated deletion of the Itgb4 (β4) gene in Schwann cells. After a crush lesion of the sciatic nerve, the recovery of motor, but not that of sensory, nerve function in β4^–/– mice was delayed. Immunostaining of neurofilament-200 showed that there also is a significant reduction in the number of newly outgrowing nerve sprouts in β4^–/– mice. Morphometric quantitative measurements revealed that fewer axons are myelinated in the nonlesioned β4^–/– nerves. After a sciatic nerve crush lesion, β4^–/– mice did not only have fewer myelinated axons compared with lesioned wild-type nerve, but their axons also showed a higher g-ratio and a thinner myelin sheath, pointing at reduced myelination. This study revealed that the β4 protein remains expressed in the early stages of peripheral regeneration, albeit at levels lower than those before the lesion was inflicted, and showed that laminin deposition is not altered in the absence of β4. These results together demonstrate that integrin 6β4 plays an essential role in axonal regeneration and subsequent myelination.

Key words: integrin; knock-out mice; sciatic nerve; Schwann cell; myelin repair; peripheral nerve

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Received Feb. 26, 2008; revised Sept. 5, 2008; accepted Sept. 9, 2008.

Correspondence should be addressed to either of the following: Dr. Catharina E. E. M. Van der Zee, Department of Cell Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Medical Center Nijmegen, Geert Groote plein 28, 6525 GA Nijmegen, The Netherlands, Email: i.vanderzee{at}ncmls.ru.nl; or Dr. Arnoud Sonnenberg, Division of Cell Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands, E-mail: Email: a.sonnenberg{at}nki.nl

This article has been cited by other articles:

				Y. Tao, P. Dai, Y. Liu, S. Marchetto, W.-C. Xiong, J.-P. Borg, and L. Mei Erbin regulates NRG1 signaling and myelination PNAS, June 9, 2009; 106(23): 9477 - 9482. [Abstract] [Full Text] [PDF]

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