SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination
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-de...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-12, Vol.9 (12), p.e115400-e115400 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e115400 |
|---|---|
| container_issue | 12 |
| container_start_page | e115400 |
| container_title | PloS one |
| container_volume | 9 |
| creator | Fujiwara, Sayaka Hoshikawa, Shinya Ueno, Takaaki Hirata, Makoto Saito, Taku Ikeda, Toshiyuki Kawaguchi, Hiroshi Nakamura, Kozo Tanaka, Sakae Ogata, Toru |
| description | 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. |
| doi_str_mv | 10.1371/journal.pone.0115400 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1640008813</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A418126275</galeid><doaj_id>oai_doaj_org_article_3791760a2df74fd895c61d02f0d722b3</doaj_id><sourcerecordid>A418126275</sourcerecordid><originalsourceid>FETCH-LOGICAL-c809t-23fc851b9c859629788e575e3ba584fe0345875ffa59eaccddae92ea76a540d33</originalsourceid><addsrcrecordid>eNqNk12L1DAUhoso7rr6D0QLgujFjPlo2vRGWBc_BhYGHBUvhJBJT2aytEk3SVf335vudJcZ2QsptOXkOe_peXtOlj3HaI5phd9duMFb2c57Z2GOMGYFQg-yY1xTMisJog_33o-yJyFcIMQoL8vH2RFhjJaEkOPs12r5E6M8emmDVNFcyQghX2GEPuTR5WHoew8hRdT2t7Q2V9C2ee9dazR4GY2zubTNiKZg5yLk3TW0xt4cPc0eadkGeDY9T7Lvnz5-O_syO19-Xpydns8UR3WcEaoVZ3hdp3tdkrriHFjFgK4l44UGRAvGK6a1ZDVIpZpGQk1AVqVMTTeUnmQvd7p964KYjAkCl8kSxDkeicWOaJy8EL03nfTXwkkjbgLOb4T00agWBK1qXJVIkkZXhW54zVSJG0Q0aipC1qPW-6nasO6gUWCTe-2B6OGJNVuxcVeiIBUjmCSBN5OAd5cDhCg6E0ZjpQU37L674JiUPKGv_kHv726iNjI1YKx2qa4aRcVpgUelVDlR83uodDXQGZWmSJsUP0h4e5CQmAh_4kYOIYjF6uv_s8sfh-zrPXYLso3b4NphHJlwCBY7UHkXggd9ZzJGYlyCWzfEuARiWoKU9mL_B90l3U49_Qsy7wCS</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1640008813</pqid></control><display><type>article</type><title>SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Fujiwara, Sayaka ; Hoshikawa, Shinya ; Ueno, Takaaki ; Hirata, Makoto ; Saito, Taku ; Ikeda, Toshiyuki ; Kawaguchi, Hiroshi ; Nakamura, Kozo ; Tanaka, Sakae ; Ogata, Toru</creator><contributor>Kursula, Petri</contributor><creatorcontrib>Fujiwara, Sayaka ; Hoshikawa, Shinya ; Ueno, Takaaki ; Hirata, Makoto ; Saito, Taku ; Ikeda, Toshiyuki ; Kawaguchi, Hiroshi ; Nakamura, Kozo ; Tanaka, Sakae ; Ogata, Toru ; Kursula, Petri</creatorcontrib><description>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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0115400</identifier><identifier>PMID: 25536222</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alzheimer's disease ; Amyotrophic lateral sclerosis ; Animals ; Base Sequence ; Biology and Life Sciences ; Biomarkers - metabolism ; Cell Differentiation ; Cell growth ; Cell Line ; Cell Proliferation ; Disorders ; Dorsal root ganglia ; Ganglia ; Gene expression ; Gene Knockdown Techniques ; Growth factors ; Humans ; Introns - genetics ; Kinases ; Medicine ; Mice ; Molecular Sequence Data ; Mutation ; Myelin P0 Protein - metabolism ; Myelin Sheath - metabolism ; Myelination ; Protein Binding - genetics ; Proteins ; Rats ; Regulatory sequences ; Response Elements - genetics ; Rodents ; S100 Calcium Binding Protein beta Subunit - genetics ; S100 Calcium Binding Protein beta Subunit - metabolism ; S100b protein ; Schwann cells ; Schwann Cells - cytology ; Schwann Cells - metabolism ; Sciatic nerve ; Signal Transduction - genetics ; Signaling ; Sox10 protein ; SOXE Transcription Factors - genetics ; SOXE Transcription Factors - metabolism ; Transcription factors ; Transcriptional Activation - genetics</subject><ispartof>PloS one, 2014-12, Vol.9 (12), p.e115400-e115400</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Fujiwara et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Fujiwara et al 2014 Fujiwara et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c809t-23fc851b9c859629788e575e3ba584fe0345875ffa59eaccddae92ea76a540d33</citedby><cites>FETCH-LOGICAL-c809t-23fc851b9c859629788e575e3ba584fe0345875ffa59eaccddae92ea76a540d33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275212/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275212/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25536222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kursula, Petri</contributor><creatorcontrib>Fujiwara, Sayaka</creatorcontrib><creatorcontrib>Hoshikawa, Shinya</creatorcontrib><creatorcontrib>Ueno, Takaaki</creatorcontrib><creatorcontrib>Hirata, Makoto</creatorcontrib><creatorcontrib>Saito, Taku</creatorcontrib><creatorcontrib>Ikeda, Toshiyuki</creatorcontrib><creatorcontrib>Kawaguchi, Hiroshi</creatorcontrib><creatorcontrib>Nakamura, Kozo</creatorcontrib><creatorcontrib>Tanaka, Sakae</creatorcontrib><creatorcontrib>Ogata, Toru</creatorcontrib><title>SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>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.</description><subject>Alzheimer's disease</subject><subject>Amyotrophic lateral sclerosis</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biology and Life Sciences</subject><subject>Biomarkers - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>Disorders</subject><subject>Dorsal root ganglia</subject><subject>Ganglia</subject><subject>Gene expression</subject><subject>Gene Knockdown Techniques</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Introns - genetics</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Myelin P0 Protein - metabolism</subject><subject>Myelin Sheath - metabolism</subject><subject>Myelination</subject><subject>Protein Binding - genetics</subject><subject>Proteins</subject><subject>Rats</subject><subject>Regulatory sequences</subject><subject>Response Elements - genetics</subject><subject>Rodents</subject><subject>S100 Calcium Binding Protein beta Subunit - genetics</subject><subject>S100 Calcium Binding Protein beta Subunit - metabolism</subject><subject>S100b protein</subject><subject>Schwann cells</subject><subject>Schwann Cells - cytology</subject><subject>Schwann Cells - metabolism</subject><subject>Sciatic nerve</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>Sox10 protein</subject><subject>SOXE Transcription Factors - genetics</subject><subject>SOXE Transcription Factors - metabolism</subject><subject>Transcription factors</subject><subject>Transcriptional Activation - genetics</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLgujFjPlo2vRGWBc_BhYGHBUvhJBJT2aytEk3SVf335vudJcZ2QsptOXkOe_peXtOlj3HaI5phd9duMFb2c57Z2GOMGYFQg-yY1xTMisJog_33o-yJyFcIMQoL8vH2RFhjJaEkOPs12r5E6M8emmDVNFcyQghX2GEPuTR5WHoew8hRdT2t7Q2V9C2ee9dazR4GY2zubTNiKZg5yLk3TW0xt4cPc0eadkGeDY9T7Lvnz5-O_syO19-Xpydns8UR3WcEaoVZ3hdp3tdkrriHFjFgK4l44UGRAvGK6a1ZDVIpZpGQk1AVqVMTTeUnmQvd7p964KYjAkCl8kSxDkeicWOaJy8EL03nfTXwkkjbgLOb4T00agWBK1qXJVIkkZXhW54zVSJG0Q0aipC1qPW-6nasO6gUWCTe-2B6OGJNVuxcVeiIBUjmCSBN5OAd5cDhCg6E0ZjpQU37L674JiUPKGv_kHv726iNjI1YKx2qa4aRcVpgUelVDlR83uodDXQGZWmSJsUP0h4e5CQmAh_4kYOIYjF6uv_s8sfh-zrPXYLso3b4NphHJlwCBY7UHkXggd9ZzJGYlyCWzfEuARiWoKU9mL_B90l3U49_Qsy7wCS</recordid><startdate>20141223</startdate><enddate>20141223</enddate><creator>Fujiwara, Sayaka</creator><creator>Hoshikawa, Shinya</creator><creator>Ueno, Takaaki</creator><creator>Hirata, Makoto</creator><creator>Saito, Taku</creator><creator>Ikeda, Toshiyuki</creator><creator>Kawaguchi, Hiroshi</creator><creator>Nakamura, Kozo</creator><creator>Tanaka, Sakae</creator><creator>Ogata, Toru</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20141223</creationdate><title>SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination</title><author>Fujiwara, Sayaka ; Hoshikawa, Shinya ; Ueno, Takaaki ; Hirata, Makoto ; Saito, Taku ; Ikeda, Toshiyuki ; Kawaguchi, Hiroshi ; Nakamura, Kozo ; Tanaka, Sakae ; Ogata, Toru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c809t-23fc851b9c859629788e575e3ba584fe0345875ffa59eaccddae92ea76a540d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Alzheimer's disease</topic><topic>Amyotrophic lateral sclerosis</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biology and Life Sciences</topic><topic>Biomarkers - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>Disorders</topic><topic>Dorsal root ganglia</topic><topic>Ganglia</topic><topic>Gene expression</topic><topic>Gene Knockdown Techniques</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Introns - genetics</topic><topic>Kinases</topic><topic>Medicine</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Myelin P0 Protein - metabolism</topic><topic>Myelin Sheath - metabolism</topic><topic>Myelination</topic><topic>Protein Binding - genetics</topic><topic>Proteins</topic><topic>Rats</topic><topic>Regulatory sequences</topic><topic>Response Elements - genetics</topic><topic>Rodents</topic><topic>S100 Calcium Binding Protein beta Subunit - genetics</topic><topic>S100 Calcium Binding Protein beta Subunit - metabolism</topic><topic>S100b protein</topic><topic>Schwann cells</topic><topic>Schwann Cells - cytology</topic><topic>Schwann Cells - metabolism</topic><topic>Sciatic nerve</topic><topic>Signal Transduction - genetics</topic><topic>Signaling</topic><topic>Sox10 protein</topic><topic>SOXE Transcription Factors - genetics</topic><topic>SOXE Transcription Factors - metabolism</topic><topic>Transcription factors</topic><topic>Transcriptional Activation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujiwara, Sayaka</creatorcontrib><creatorcontrib>Hoshikawa, Shinya</creatorcontrib><creatorcontrib>Ueno, Takaaki</creatorcontrib><creatorcontrib>Hirata, Makoto</creatorcontrib><creatorcontrib>Saito, Taku</creatorcontrib><creatorcontrib>Ikeda, Toshiyuki</creatorcontrib><creatorcontrib>Kawaguchi, Hiroshi</creatorcontrib><creatorcontrib>Nakamura, Kozo</creatorcontrib><creatorcontrib>Tanaka, Sakae</creatorcontrib><creatorcontrib>Ogata, Toru</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujiwara, Sayaka</au><au>Hoshikawa, Shinya</au><au>Ueno, Takaaki</au><au>Hirata, Makoto</au><au>Saito, Taku</au><au>Ikeda, Toshiyuki</au><au>Kawaguchi, Hiroshi</au><au>Nakamura, Kozo</au><au>Tanaka, Sakae</au><au>Ogata, Toru</au><au>Kursula, Petri</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-12-23</date><risdate>2014</risdate><volume>9</volume><issue>12</issue><spage>e115400</spage><epage>e115400</epage><pages>e115400-e115400</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25536222</pmid><doi>10.1371/journal.pone.0115400</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-12, Vol.9 (12), p.e115400-e115400 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1640008813 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Alzheimer's disease Amyotrophic lateral sclerosis Animals Base Sequence Biology and Life Sciences Biomarkers - metabolism Cell Differentiation Cell growth Cell Line Cell Proliferation Disorders Dorsal root ganglia Ganglia Gene expression Gene Knockdown Techniques Growth factors Humans Introns - genetics Kinases Medicine Mice Molecular Sequence Data Mutation Myelin P0 Protein - metabolism Myelin Sheath - metabolism Myelination Protein Binding - genetics Proteins Rats Regulatory sequences Response Elements - genetics Rodents S100 Calcium Binding Protein beta Subunit - genetics S100 Calcium Binding Protein beta Subunit - metabolism S100b protein Schwann cells Schwann Cells - cytology Schwann Cells - metabolism Sciatic nerve Signal Transduction - genetics Signaling Sox10 protein SOXE Transcription Factors - genetics SOXE Transcription Factors - metabolism Transcription factors Transcriptional Activation - genetics |
| title | SOX10 transactivates S100B to suppress Schwann cell proliferation and to promote myelination |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T08%3A28%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=SOX10%20transactivates%20S100B%20to%20suppress%20Schwann%20cell%20proliferation%20and%20to%20promote%20myelination&rft.jtitle=PloS%20one&rft.au=Fujiwara,%20Sayaka&rft.date=2014-12-23&rft.volume=9&rft.issue=12&rft.spage=e115400&rft.epage=e115400&rft.pages=e115400-e115400&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0115400&rft_dat=%3Cgale_plos_%3EA418126275%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1640008813&rft_id=info:pmid/25536222&rft_galeid=A418126275&rft_doaj_id=oai_doaj_org_article_3791760a2df74fd895c61d02f0d722b3&rfr_iscdi=true |