Schwann cells synthesize α7β1 integrin which is dispensable for peripheral nerve development and myelination

Abstract

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, α7β1 integrin, previously described only in neurons, is also expressed in Schwann cells. The expression of α7 appears postnatally, such that α7β1 is the last laminin receptor expressed by differentiating Schwann cells. Genetic inactivation of the α7 subunit in mice does not affect peripheral nerve formation or the expression of other laminin receptors. Of note, α7β1 is not necessary for basal lamina formation and myelination. Nonetheless, these data taken together with the previous demonstration of impaired axonal regrowth in α7-null mice suggest a possible Schwann cell-autonomous role for α7 in nerve regeneration.