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SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro
► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidati...
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| Published in: | Neuroscience letters 2011-09, Vol.503 (1), p.10-14 |
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| creator | Veiga, S. Ly, J. Chan, P.H. Bresnahan, J.C. Beattie, M.S. |
| description | ► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidative stress-mediated death.
Spinal cord injury (SCI) produces a significant loss of oligodendrocytes (OL) and demyelination. The oligodendrocyte precursor cells (OPCs) response includes a group of cellular changes in OPCs that are directed to replenish OL loss from the injury. However, this adaptive response is hampered and OPCs eventually die or fail to differentiate to mature and functional OL. In this study, we wanted to evaluate if overexpression of human superoxide dismutase 1 (hSOD1) in OPCs from the SOD1 transgenic rat could improve some of the features of the OPC response in vitro. We found that hSOD1 overexpression increases the proliferation of OPCs and accelerates their differentiation to mature OL in vitro. Furthermore, hSOD1 overexpression reduces oxidative stress-mediated death in OPCs. These results suggest hSOD1 as a therapeutic target to increase OPC response success and potentially, OL replacement and remyelination after SCI. |
| doi_str_mv | 10.1016/j.neulet.2011.07.053 |
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Spinal cord injury (SCI) produces a significant loss of oligodendrocytes (OL) and demyelination. The oligodendrocyte precursor cells (OPCs) response includes a group of cellular changes in OPCs that are directed to replenish OL loss from the injury. However, this adaptive response is hampered and OPCs eventually die or fail to differentiate to mature and functional OL. In this study, we wanted to evaluate if overexpression of human superoxide dismutase 1 (hSOD1) in OPCs from the SOD1 transgenic rat could improve some of the features of the OPC response in vitro. We found that hSOD1 overexpression increases the proliferation of OPCs and accelerates their differentiation to mature OL in vitro. Furthermore, hSOD1 overexpression reduces oxidative stress-mediated death in OPCs. These results suggest hSOD1 as a therapeutic target to increase OPC response success and potentially, OL replacement and remyelination after SCI.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2011.07.053</identifier><identifier>PMID: 21843597</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Analysis of Variance ; Animals ; Biological and medical sciences ; Bromodeoxyuridine - metabolism ; CD11b Antigen - metabolism ; Cell Count ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell Proliferation - drug effects ; Cells, Cultured ; Cerebral Cortex - cytology ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; Gangliosides - metabolism ; Humans ; Intercellular Signaling Peptides and Proteins - pharmacology ; Myelin Basic Protein - metabolism ; Oligodendrocyte differentiation ; Oligodendroglia - drug effects ; Oligodendroglia - physiology ; OPC proliferation ; OPC response ; Oxidative stress ; Rats ; Rats, Sprague-Dawley ; Rats, Transgenic ; Stem Cells - drug effects ; Stem Cells - physiology ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxide Dismutase-1 ; tert-Butylhydroperoxide - pharmacology ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2011-09, Vol.503 (1), p.10-14</ispartof><rights>2011 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><rights>2011 Elsevier Ireland Ltd. All rights reserved. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-7b31e2c29aa85a492b7ea46d971fbfea2fb483c79e2150d9440ade318198c9a43</citedby><cites>FETCH-LOGICAL-c524t-7b31e2c29aa85a492b7ea46d971fbfea2fb483c79e2150d9440ade318198c9a43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24523096$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21843597$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Veiga, S.</creatorcontrib><creatorcontrib>Ly, J.</creatorcontrib><creatorcontrib>Chan, P.H.</creatorcontrib><creatorcontrib>Bresnahan, J.C.</creatorcontrib><creatorcontrib>Beattie, M.S.</creatorcontrib><title>SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidative stress-mediated death.
Spinal cord injury (SCI) produces a significant loss of oligodendrocytes (OL) and demyelination. The oligodendrocyte precursor cells (OPCs) response includes a group of cellular changes in OPCs that are directed to replenish OL loss from the injury. However, this adaptive response is hampered and OPCs eventually die or fail to differentiate to mature and functional OL. In this study, we wanted to evaluate if overexpression of human superoxide dismutase 1 (hSOD1) in OPCs from the SOD1 transgenic rat could improve some of the features of the OPC response in vitro. We found that hSOD1 overexpression increases the proliferation of OPCs and accelerates their differentiation to mature OL in vitro. Furthermore, hSOD1 overexpression reduces oxidative stress-mediated death in OPCs. These results suggest hSOD1 as a therapeutic target to increase OPC response success and potentially, OL replacement and remyelination after SCI.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bromodeoxyuridine - metabolism</subject><subject>CD11b Antigen - metabolism</subject><subject>Cell Count</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gangliosides - metabolism</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - pharmacology</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Oligodendrocyte differentiation</subject><subject>Oligodendroglia - drug effects</subject><subject>Oligodendroglia - physiology</subject><subject>OPC proliferation</subject><subject>OPC response</subject><subject>Oxidative stress</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Transgenic</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - physiology</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase-1</subject><subject>tert-Butylhydroperoxide - pharmacology</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kcFu1DAQhi0EokvhDRDyBXFK8NhOHF-QUAsFqVIPgMTNcpxJ61XWDnayat8eV7u0cOFkafz9M2N_hLwGVgOD9v22DrhOuNScAdRM1awRT8gGOsUrpRV_SjZMMFkJLdkJeZHzljHWQCOfkxMOnRSNVhvy89vVOdC4x4S3c8KcfQzU7-ZUSpmOaJe1VGkc6XKDNE7-Og4YhhTd3YK0JNyacky0QHMMGakPdO-XFF-SZ6OdMr46nqfkx-dP38--VJdXF1_PPl5WruFyqVQvALnj2tqusVLzXqGV7aAVjH0Zz8dedsIpjRwaNmgpmR1QQAe6c9pKcUo-HPrOa7_DwWFYkp3MnPzOpjsTrTf_3gR_Y67j3ghQ0EBXGrw7Nkjx14p5MTufHU6TDRjXbDRT0KpW60LKA-lSzDnh-DAFmLl3Yrbm4MTcOzFMmeKkxN78veFD6I-EArw9AjY7O43JBufzIycbLphuH5-K5T_3HpPJzmNwOPjiYTFD9P_f5Dc4bK94</recordid><startdate>20110926</startdate><enddate>20110926</enddate><creator>Veiga, S.</creator><creator>Ly, J.</creator><creator>Chan, P.H.</creator><creator>Bresnahan, J.C.</creator><creator>Beattie, M.S.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>5PM</scope></search><sort><creationdate>20110926</creationdate><title>SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro</title><author>Veiga, S. ; Ly, J. ; Chan, P.H. ; Bresnahan, J.C. ; Beattie, M.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-7b31e2c29aa85a492b7ea46d971fbfea2fb483c79e2150d9440ade318198c9a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bromodeoxyuridine - metabolism</topic><topic>CD11b Antigen - metabolism</topic><topic>Cell Count</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gangliosides - metabolism</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - pharmacology</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Oligodendrocyte differentiation</topic><topic>Oligodendroglia - drug effects</topic><topic>Oligodendroglia - physiology</topic><topic>OPC proliferation</topic><topic>OPC response</topic><topic>Oxidative stress</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Transgenic</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - physiology</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxide Dismutase-1</topic><topic>tert-Butylhydroperoxide - pharmacology</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Veiga, S.</creatorcontrib><creatorcontrib>Ly, J.</creatorcontrib><creatorcontrib>Chan, P.H.</creatorcontrib><creatorcontrib>Bresnahan, J.C.</creatorcontrib><creatorcontrib>Beattie, M.S.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Veiga, S.</au><au>Ly, J.</au><au>Chan, P.H.</au><au>Bresnahan, J.C.</au><au>Beattie, M.S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2011-09-26</date><risdate>2011</risdate><volume>503</volume><issue>1</issue><spage>10</spage><epage>14</epage><pages>10-14</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>► Overexpression of hSOD1 increases proliferation rate and oligodendrocyte precursor cells (OPCs) in vitro. ► SOD1 overexpression in OPCs accelerates the acquisition of a mature oligodendrocyte (OL) phenotype in vitro. ► Overexpression of hSOD1 in OPCs, but not mature OLs, rescues cells from oxidative stress-mediated death.
Spinal cord injury (SCI) produces a significant loss of oligodendrocytes (OL) and demyelination. The oligodendrocyte precursor cells (OPCs) response includes a group of cellular changes in OPCs that are directed to replenish OL loss from the injury. However, this adaptive response is hampered and OPCs eventually die or fail to differentiate to mature and functional OL. In this study, we wanted to evaluate if overexpression of human superoxide dismutase 1 (hSOD1) in OPCs from the SOD1 transgenic rat could improve some of the features of the OPC response in vitro. We found that hSOD1 overexpression increases the proliferation of OPCs and accelerates their differentiation to mature OL in vitro. Furthermore, hSOD1 overexpression reduces oxidative stress-mediated death in OPCs. These results suggest hSOD1 as a therapeutic target to increase OPC response success and potentially, OL replacement and remyelination after SCI.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>21843597</pmid><doi>10.1016/j.neulet.2011.07.053</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuroscience letters, 2011-09, Vol.503 (1), p.10-14 |
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| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | Analysis of Variance Animals Biological and medical sciences Bromodeoxyuridine - metabolism CD11b Antigen - metabolism Cell Count Cell Differentiation - drug effects Cell Differentiation - genetics Cell Proliferation - drug effects Cells, Cultured Cerebral Cortex - cytology Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Gangliosides - metabolism Humans Intercellular Signaling Peptides and Proteins - pharmacology Myelin Basic Protein - metabolism Oligodendrocyte differentiation Oligodendroglia - drug effects Oligodendroglia - physiology OPC proliferation OPC response Oxidative stress Rats Rats, Sprague-Dawley Rats, Transgenic Stem Cells - drug effects Stem Cells - physiology Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase-1 tert-Butylhydroperoxide - pharmacology Time Factors Vertebrates: nervous system and sense organs |
| title | SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro |
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