{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,21]],"date-time":"2025-09-21T18:32:34Z","timestamp":1758479554430},"reference-count":73,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2001,9,26]],"date-time":"2001-09-26T00:00:00Z","timestamp":1001462400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Association Fran\u00e7aise contre les Myopathies"},{"name":"Association pour la Recherche sur la Scl\u00e9rose en Plaques"},{"name":"Pasteur-Weizmann Joint Research Program"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2001,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The discovery that the dominant X\u2010linked form of Charcot\u2010Marie\u2010Tooth disease (CMTX), a genetic disease of the peripheral nervous system (PNS), is associated with mutations in connexin32 (Cx32) has brought attention to the importance of connexins in glial cell biology. To gain further insight into the consequences of Cx32 deficiency, we have undertaken a detailed characterization of the gene expression profile of Schwann cells isolated from the sciatic nerve of wild\u2010type and Cx32\u2010null mice. Schwann cells exhibit two distinct phenotypes, myelinating and nonmyelinating, which are defined by their different morphology with respect to axons and by their unique profile of gene expression. Our findings show that, regardless of the mouse genotype, cultured Schwann cells express similar levels of messages for a number of connexins and for genes characteristic of both the myelinating and the nonmyelinating phenotypes. Furthermore, we have identified Cx36, a member of the \u03b3 subclass of connexins, which are preferentially expressed in neuronal cells of mouse brain and retina, as an additional connexin present in Schwann cells. Mice lacking Cx32, however, exhibited a marked up\u2010regulation of glial fibrillary acidic protein (GFAP), a cytoskeletal protein usually synthesized only by nonmyelinating Schwann cells. This observation was extended to the PNS in vivo and did not reflect a general perturbation of the expression of other nonmyelinating Schwann cell genes. These findings demonstrate that the absence of Cx32 results in a distinct pattern of gene dysregulation in Schwann cells and that Schwann cell homeostasis is critically dependent on the correct expression of Cx32 and not just any connexin. Identifying the relationship between increased GFAP expression and the absence of Cx32 could lead to the definition of specific roles for Cx32 in the control of myelin homeostasis and in the development of CMTX. J. Neurosci. Res. 66:23\u201336, 2001. \u00a9 2001 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.1194","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T19:55:21Z","timestamp":1030305321000},"page":"23-36","source":"Crossref","is-referenced-by-count":21,"title":["Altered gene expression in Schwann cells of connexin32 knockout animals"],"prefix":"10.1002","volume":"66","author":[{"given":"Simone M.","family":"Nicholson","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Danielle","family":"Gom\u00e8s","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B\u00e9atrice","family":"de 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