Dorsal root ganglion neurons up-regulate the expression of laminin-associated integrins after peripheral but not central axotomy
✍ Scribed by Wilhelm Wallquist; Johan Zelano; Stefan Plantman; Stephen J. Kaufman; Staffan Cullheim; Henrik Hammarberg
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 421 KB
- Volume
- 480
- Category
- Article
- ISSN
- 0021-9967
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✦ Synopsis
Abstract
The favorable prognosis of regeneration in the peripheral nervous system after axonal lesions is generally regarded as dependent on the Schwann cell basal lamina. Laminins, a heterotrimeric group of basal lamina molecules, have been suggested to be among the factors playing this supportive role. For neurons to utilize laminin as a substrate for growth, an expression of laminin binding receptors, integrins, is necessary. In this study, we have examined the expression of laminin binding integrin subunits in dorsal root ganglion (DRG) neurons after transection to either their peripherally projecting axons, as in the sciatic nerve, followed by regeneration, or the centrally projecting axons in dorsal roots, followed by no or weak regenerative activity. In uninjured DRG, immunohistochemical staining revealed a few neurons expressing integrin subunit α6, whereas integrin subunits α7 and foremost β1 were expressed in a majority of neurons. After an injury to the sciatic nerve, mRNAs encoding all three integrins were up‐regulated in DRG neurons. By anterograde tracing, immunoreactivity for all studied integrins was also found in association with growing axons after a sciatic nerve crush lesion in vivo. In contrast, mRNA levels remained constant in DRG neurons after a dorsal root injury. Together with previous findings, this suggests that integrin subunits α6, α7, and β1 have an important role in the regenerative response following nerve injury and that the lack of regenerative capacity following dorsal root injury could in part be explained by the absence of response in integrin regulation. J. Comp. Neurol. 480:162–169, 2004. © 2004 Wiley‐Liss, Inc.