Titre
Sox4 participates in the modulation of Schwann cell myelination.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Bartesaghi, L.
Auteure/Auteur
Arnaud Gouttenoire, E.
Auteure/Auteur
Prunotto, A.
Auteure/Auteur
Médard, J.J.
Auteure/Auteur
Bergmann, S.
Auteure/Auteur
Chrast, R.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1460-9568
Statut éditorial
Publié
Date de publication
2015
Volume
42
Numéro
2
Première page
1788
Dernière page/numéro d’article
1796
Peer-reviewed
Oui
Langue
anglais
Résumé
In order to identify new regulators of Schwann cell myelination potentially playing a role in peripheral nervous system (PNS) pathologies, we analysed gene expression profiling data from three mouse models of demyelinating neuropathies and from the developing PNS. This analysis revealed that Sox4, which encodes a member of the Sry-related high-mobility group box protein family, was consistently upregulated in all three analysed models of neuropathy. Moreover, Sox4 showed a peak in its expression during development that corresponded with the onset of myelination. To gain further insights into the role of Sox4 in PNS development, we generated a transgenic mouse that specifically overexpresses Sox4 in Schwann cells. Sox4 overexpression led to a temporary delay in PNS myelination without affecting axonal sorting. Importantly, we observed that, whereas Sox4 mRNA could be efficiently overexpressed, Sox4 protein expression in Schwann cells was strictly regulated. Finally, our data showed that enforced expression of Sox4 in the mouse model for Charcot-Marie-Tooth 4C aggravated its neuropathic phenotype. Together, these observations reveal that Sox4 contributes to the regulation of Schwann cell myelination, and also indicates its involvement in the pathophysiology of peripheral neuropathies.
Sujets
PID Serval
serval:BIB_DF6145E49C9F
PMID
Date de création
2015-08-24T15:46:22.115Z
Date de création dans IRIS
2025-05-21T05:58:16Z