| First Author | Previtali SC | Year | 2003 |
| Journal | Mol Cell Neurosci | Volume | 23 |
| Issue | 2 | Pages | 210-8 |
| PubMed ID | 12812754 | Mgi Jnum | J:83980 |
| Mgi Id | MGI:2664470 | Doi | 10.1016/s1044-7431(03)00014-9 |
| Citation | Previtali SC, et al. (2003) Schwann cells synthesize alpha7beta1 integrin which is dispensable for peripheral nerve development and myelination. Mol Cell Neurosci 23(2):210-8 |
| abstractText | Defects in laminins or laminin receptors are responsible for various neuromuscular disorders, including peripheral neuropathies. Interactions between Schwann cells and their basal lamina are fundamental to peripheral nerve development and successful myelination. Selected laminins are expressed in the endoneurium, and their receptors are developmentally regulated during peripheral nerve formation. Loss-of-function mutations have confirmed the importance and the role of some of these molecules. Here we show for the first time that another laminin receptor, alpha7beta1 integrin, previously described only in neurons, is also expressed in Schwann cells. The expression of alpha7 appears postnatally, such that alpha7beta1 is the last laminin receptor expressed by differentiating Schwann cells. Genetic inactivation of the alpha7 subunit in mice does not affect peripheral nerve formation or the expression of other laminin receptors. Of note, alpha7beta1 is not necessary for basal lamina formation and myelination. Nonetheless, these data taken together with the previous demonstration of impaired axonal regrowth in alpha7-null mice suggest a possible Schwann cell-autonomous role for alpha7 in nerve regeneration. |
