SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination.

Authors: Fujiwara, Sayaka  Hoshikawa, Shinya  Ueno, Takaaki  Hirata, Makoto  Saito, Taku  Ikeda, Toshiyuki  Kawaguchi, Hiroshi  Nakamura, Kozo  Tanaka, Sakae  Ogata, Toru 
Citation: Fujiwara S, etal., PLoS One. 2014 Dec 23;9(12):e115400. doi: 10.1371/journal.pone.0115400. eCollection 2014.
Pubmed: (View Article at PubMed) PMID:25536222
DOI: Full-text: DOI:10.1371/journal.pone.0115400

Schwann cells are an important cell source for regenerative therapy for neural disorders. We investigated the role of the transcription factor sex determining region Y (SRY)-box 10 (SOX10) in the proliferation and myelination of Schwann cells. SOX10 is predominantly expressed in rat sciatic nerve-derived Schwann cells and is induced shortly after birth. Among transcription factors known to be important for the differentiation of Schwann cells, SOX10 potently transactivates the S100B promoter. In cultures of Schwann cells, overexpressing SOX10 dramatically induces S100B expression, while knocking down SOX10 with shRNA suppresses S100B expression. Here, we identify three core response elements of SOX10 in the S100B promoter and intron 1 with a putative SOX motif. Knockdown of either SOX10 or S100B enhances the proliferation of Schwann cells. In addition, using dissociated cultures of dorsal root ganglia, we demonstrate that suppressing S100B with shRNA impairs myelination of Schwann cells. These results suggest that the SOX10-S100B signaling axis critically regulates Schwann cell proliferation and myelination, and therefore is a putative therapeutic target for neuronal disorders.

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CRRD ID: 12879826
Created: 2017-04-26
Species: All species
Last Modified: 2017-04-26
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.