Evidence that nuclear factor IA inhibits repair after white matter injury
Objective: Chronic demyelination can result in axonopathy and is associated with human neurological conditions such as multiple sclerosis (MS) in adults and cerebral palsy in infants. In these disorders, myelin regeneration is inhibited by impaired differentiation of oligodendrocyte progenitors into...
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| Veröffentlicht in: | Annals of neurology 2012-08, Vol.72 (2), p.224-233 |
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| container_title | Annals of neurology |
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| creator | Fancy, Stephen P. J. Glasgow, Stacey M. Finley, Meggie Rowitch, David H. Deneen, Benjamin |
| description | Objective:
Chronic demyelination can result in axonopathy and is associated with human neurological conditions such as multiple sclerosis (MS) in adults and cerebral palsy in infants. In these disorders, myelin regeneration is inhibited by impaired differentiation of oligodendrocyte progenitors into myelin‐producing oligodendrocytes. However, regulatory factors relevant in human myelin disorders and in myelin regeneration remain poorly understood. Here we have investigated the role of the transcription factor nuclear factor IA (NFIA) in oligodendrocyte progenitor differentiation during developmental and regenerative myelination.
Methods:
NFIA expression patterns in human neonatal hypoxic–ischemic encephalopathy (HIE) and MS as well as developmental expression in mice were evaluated. Functional studies during remyelination were performed using a lysolecithin model, coupled with lentiviral misexpression of NFIA. The role of NFIA during oligodendrocyte lineage development was characterized using chick and mouse models and in vitro culture of oligodendrocyte progenitors. Biochemical mechanism of NFIA function was evaluated using chromatin immunoprecipitation and reporter assays.
Results:
NFIA is expressed in oligodendrocyte progenitors, but not differentiated oligodendrocytes during mouse embryonic development. Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE, as well active MS lesions in adults, revealed that it is similarly expressed in oligodendrocyte progenitors and not oligodendrocytes. Functional studies indicate that NFIA is sufficient to suppress oligodendrocyte progenitor differentiation during adult remyelination and embryonic development through direct repression of myelin gene expression.
Interpretation:
These studies suggest that NFIA participates in the control of oligodendrocyte progenitor differentiation and may contribute to the inhibition of remyelination in human myelin disorders. ANN NEUROL 2012; |
| doi_str_mv | 10.1002/ana.23590 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1520390823</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3276332241</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4890-d529a3faeaba93fbbc47f92d41ec0d906972f4162de674658f697a78d7601d263</originalsourceid><addsrcrecordid>eNp10N9rFDEQB_Agij2rD_4DEpCCPmw7-bHZzeNZaj0oFUER-hJmswmXc2_3TLKt99-7510rFPo0ZPjMTPgS8pbBKQPgZ9jjKRelhmdkxkrBippL_ZzMQChZlEzII_IqpRUAaMXgJTnivIZKMJiRxcVtaF1vHc1LzLQfbecwUo82D5Eu5jT0y9CEnGh0GwyRos8u0rtlyI6uMe8eoV-NcfuavPDYJffmUI_Jj88X38-_FFdfLxfn86vCylpD0ZZco_DosEEtfNNYWXnNW8mchVaD0hX3kineOlVJVdZ-6mBVt5UC1nIljsmH_d5NHH6PLmWzDsm6rsPeDWMyrOQgNNRcTPT9I7oaxthPv5sUU7KqJdOT-rhXNg4pRefNJoY1xq1hYHb5milf8y_fyb47bBybtWsf5H2gEzg5AEwWOx-xtyH9d0oIrtTOne3dXejc9umLZn49vz9d7CdCyu7PwwTGX0ZVoirNz-tLU_NPmrGbG_NN_AXUmZ4w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1516478419</pqid></control><display><type>article</type><title>Evidence that nuclear factor IA inhibits repair after white matter injury</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Fancy, Stephen P. J. ; Glasgow, Stacey M. ; Finley, Meggie ; Rowitch, David H. ; Deneen, Benjamin</creator><creatorcontrib>Fancy, Stephen P. J. ; Glasgow, Stacey M. ; Finley, Meggie ; Rowitch, David H. ; Deneen, Benjamin</creatorcontrib><description>Objective:
Chronic demyelination can result in axonopathy and is associated with human neurological conditions such as multiple sclerosis (MS) in adults and cerebral palsy in infants. In these disorders, myelin regeneration is inhibited by impaired differentiation of oligodendrocyte progenitors into myelin‐producing oligodendrocytes. However, regulatory factors relevant in human myelin disorders and in myelin regeneration remain poorly understood. Here we have investigated the role of the transcription factor nuclear factor IA (NFIA) in oligodendrocyte progenitor differentiation during developmental and regenerative myelination.
Methods:
NFIA expression patterns in human neonatal hypoxic–ischemic encephalopathy (HIE) and MS as well as developmental expression in mice were evaluated. Functional studies during remyelination were performed using a lysolecithin model, coupled with lentiviral misexpression of NFIA. The role of NFIA during oligodendrocyte lineage development was characterized using chick and mouse models and in vitro culture of oligodendrocyte progenitors. Biochemical mechanism of NFIA function was evaluated using chromatin immunoprecipitation and reporter assays.
Results:
NFIA is expressed in oligodendrocyte progenitors, but not differentiated oligodendrocytes during mouse embryonic development. Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE, as well active MS lesions in adults, revealed that it is similarly expressed in oligodendrocyte progenitors and not oligodendrocytes. Functional studies indicate that NFIA is sufficient to suppress oligodendrocyte progenitor differentiation during adult remyelination and embryonic development through direct repression of myelin gene expression.
Interpretation:
These studies suggest that NFIA participates in the control of oligodendrocyte progenitor differentiation and may contribute to the inhibition of remyelination in human myelin disorders. ANN NEUROL 2012;</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.23590</identifier><identifier>PMID: 22807310</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adenomatous Polyposis Coli Protein - metabolism ; Animals ; Arabidopsis Proteins - metabolism ; Biological and medical sciences ; Cell Differentiation - drug effects ; Cells, Cultured ; Cerebral Cortex - cytology ; Chromatin Immunoprecipitation ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Electroporation ; Embryo, Mammalian ; Gene expression ; Gene Expression Regulation, Developmental - genetics ; Gene Expression Regulation, Developmental - physiology ; Homeodomain Proteins - metabolism ; Humans ; Hypoxia-Ischemia, Brain - metabolism ; Infant ; Infant, Newborn ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Intramolecular Transferases - metabolism ; Leukoencephalopathies - chemically induced ; Leukoencephalopathies - metabolism ; Leukoencephalopathies - pathology ; Lysophosphatidylcholines - toxicity ; Medical research ; Medical sciences ; Mice ; Mice, Transgenic ; Multiple Sclerosis - metabolism ; Myelin Basic Protein - metabolism ; Neurology ; NFI Transcription Factors - genetics ; NFI Transcription Factors - metabolism ; Oligodendroglia - drug effects ; Oligodendroglia - metabolism ; Rodents ; Spinal Cord - pathology ; Stem Cells - drug effects ; Stem Cells - metabolism ; Time Factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Traumas. Diseases due to physical agents</subject><ispartof>Annals of neurology, 2012-08, Vol.72 (2), p.224-233</ispartof><rights>Copyright © 2012 American Neurological Association</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 American Neurological Association.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4890-d529a3faeaba93fbbc47f92d41ec0d906972f4162de674658f697a78d7601d263</citedby><cites>FETCH-LOGICAL-c4890-d529a3faeaba93fbbc47f92d41ec0d906972f4162de674658f697a78d7601d263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.23590$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.23590$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26332660$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22807310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fancy, Stephen P. J.</creatorcontrib><creatorcontrib>Glasgow, Stacey M.</creatorcontrib><creatorcontrib>Finley, Meggie</creatorcontrib><creatorcontrib>Rowitch, David H.</creatorcontrib><creatorcontrib>Deneen, Benjamin</creatorcontrib><title>Evidence that nuclear factor IA inhibits repair after white matter injury</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>Objective:
Chronic demyelination can result in axonopathy and is associated with human neurological conditions such as multiple sclerosis (MS) in adults and cerebral palsy in infants. In these disorders, myelin regeneration is inhibited by impaired differentiation of oligodendrocyte progenitors into myelin‐producing oligodendrocytes. However, regulatory factors relevant in human myelin disorders and in myelin regeneration remain poorly understood. Here we have investigated the role of the transcription factor nuclear factor IA (NFIA) in oligodendrocyte progenitor differentiation during developmental and regenerative myelination.
Methods:
NFIA expression patterns in human neonatal hypoxic–ischemic encephalopathy (HIE) and MS as well as developmental expression in mice were evaluated. Functional studies during remyelination were performed using a lysolecithin model, coupled with lentiviral misexpression of NFIA. The role of NFIA during oligodendrocyte lineage development was characterized using chick and mouse models and in vitro culture of oligodendrocyte progenitors. Biochemical mechanism of NFIA function was evaluated using chromatin immunoprecipitation and reporter assays.
Results:
NFIA is expressed in oligodendrocyte progenitors, but not differentiated oligodendrocytes during mouse embryonic development. Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE, as well active MS lesions in adults, revealed that it is similarly expressed in oligodendrocyte progenitors and not oligodendrocytes. Functional studies indicate that NFIA is sufficient to suppress oligodendrocyte progenitor differentiation during adult remyelination and embryonic development through direct repression of myelin gene expression.
Interpretation:
These studies suggest that NFIA participates in the control of oligodendrocyte progenitor differentiation and may contribute to the inhibition of remyelination in human myelin disorders. ANN NEUROL 2012;</description><subject>Adenomatous Polyposis Coli Protein - metabolism</subject><subject>Animals</subject><subject>Arabidopsis Proteins - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - drug effects</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Chromatin Immunoprecipitation</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Electroporation</subject><subject>Embryo, Mammalian</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Gene Expression Regulation, Developmental - physiology</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Hypoxia-Ischemia, Brain - metabolism</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Intramolecular Transferases - metabolism</subject><subject>Leukoencephalopathies - chemically induced</subject><subject>Leukoencephalopathies - metabolism</subject><subject>Leukoencephalopathies - pathology</subject><subject>Lysophosphatidylcholines - toxicity</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Multiple Sclerosis - metabolism</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Neurology</subject><subject>NFI Transcription Factors - genetics</subject><subject>NFI Transcription Factors - metabolism</subject><subject>Oligodendroglia - drug effects</subject><subject>Oligodendroglia - metabolism</subject><subject>Rodents</subject><subject>Spinal Cord - pathology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - metabolism</subject><subject>Time Factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10N9rFDEQB_Agij2rD_4DEpCCPmw7-bHZzeNZaj0oFUER-hJmswmXc2_3TLKt99-7510rFPo0ZPjMTPgS8pbBKQPgZ9jjKRelhmdkxkrBippL_ZzMQChZlEzII_IqpRUAaMXgJTnivIZKMJiRxcVtaF1vHc1LzLQfbecwUo82D5Eu5jT0y9CEnGh0GwyRos8u0rtlyI6uMe8eoV-NcfuavPDYJffmUI_Jj88X38-_FFdfLxfn86vCylpD0ZZco_DosEEtfNNYWXnNW8mchVaD0hX3kineOlVJVdZ-6mBVt5UC1nIljsmH_d5NHH6PLmWzDsm6rsPeDWMyrOQgNNRcTPT9I7oaxthPv5sUU7KqJdOT-rhXNg4pRefNJoY1xq1hYHb5milf8y_fyb47bBybtWsf5H2gEzg5AEwWOx-xtyH9d0oIrtTOne3dXejc9umLZn49vz9d7CdCyu7PwwTGX0ZVoirNz-tLU_NPmrGbG_NN_AXUmZ4w</recordid><startdate>201208</startdate><enddate>201208</enddate><creator>Fancy, Stephen P. J.</creator><creator>Glasgow, Stacey M.</creator><creator>Finley, Meggie</creator><creator>Rowitch, David H.</creator><creator>Deneen, Benjamin</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7U7</scope><scope>C1K</scope><scope>K9.</scope></search><sort><creationdate>201208</creationdate><title>Evidence that nuclear factor IA inhibits repair after white matter injury</title><author>Fancy, Stephen P. J. ; Glasgow, Stacey M. ; Finley, Meggie ; Rowitch, David H. ; Deneen, Benjamin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4890-d529a3faeaba93fbbc47f92d41ec0d906972f4162de674658f697a78d7601d263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenomatous Polyposis Coli Protein - metabolism</topic><topic>Animals</topic><topic>Arabidopsis Proteins - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - drug effects</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Chromatin Immunoprecipitation</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Electroporation</topic><topic>Embryo, Mammalian</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Developmental - genetics</topic><topic>Gene Expression Regulation, Developmental - physiology</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Hypoxia-Ischemia, Brain - metabolism</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Intramolecular Transferases - metabolism</topic><topic>Leukoencephalopathies - chemically induced</topic><topic>Leukoencephalopathies - metabolism</topic><topic>Leukoencephalopathies - pathology</topic><topic>Lysophosphatidylcholines - toxicity</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Multiple Sclerosis - metabolism</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Neurology</topic><topic>NFI Transcription Factors - genetics</topic><topic>NFI Transcription Factors - metabolism</topic><topic>Oligodendroglia - drug effects</topic><topic>Oligodendroglia - metabolism</topic><topic>Rodents</topic><topic>Spinal Cord - pathology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - metabolism</topic><topic>Time Factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fancy, Stephen P. J.</creatorcontrib><creatorcontrib>Glasgow, Stacey M.</creatorcontrib><creatorcontrib>Finley, Meggie</creatorcontrib><creatorcontrib>Rowitch, David H.</creatorcontrib><creatorcontrib>Deneen, Benjamin</creatorcontrib><collection>Istex</collection><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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fancy, Stephen P. J.</au><au>Glasgow, Stacey M.</au><au>Finley, Meggie</au><au>Rowitch, David H.</au><au>Deneen, Benjamin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence that nuclear factor IA inhibits repair after white matter injury</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2012-08</date><risdate>2012</risdate><volume>72</volume><issue>2</issue><spage>224</spage><epage>233</epage><pages>224-233</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>Objective:
Chronic demyelination can result in axonopathy and is associated with human neurological conditions such as multiple sclerosis (MS) in adults and cerebral palsy in infants. In these disorders, myelin regeneration is inhibited by impaired differentiation of oligodendrocyte progenitors into myelin‐producing oligodendrocytes. However, regulatory factors relevant in human myelin disorders and in myelin regeneration remain poorly understood. Here we have investigated the role of the transcription factor nuclear factor IA (NFIA) in oligodendrocyte progenitor differentiation during developmental and regenerative myelination.
Methods:
NFIA expression patterns in human neonatal hypoxic–ischemic encephalopathy (HIE) and MS as well as developmental expression in mice were evaluated. Functional studies during remyelination were performed using a lysolecithin model, coupled with lentiviral misexpression of NFIA. The role of NFIA during oligodendrocyte lineage development was characterized using chick and mouse models and in vitro culture of oligodendrocyte progenitors. Biochemical mechanism of NFIA function was evaluated using chromatin immunoprecipitation and reporter assays.
Results:
NFIA is expressed in oligodendrocyte progenitors, but not differentiated oligodendrocytes during mouse embryonic development. Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE, as well active MS lesions in adults, revealed that it is similarly expressed in oligodendrocyte progenitors and not oligodendrocytes. Functional studies indicate that NFIA is sufficient to suppress oligodendrocyte progenitor differentiation during adult remyelination and embryonic development through direct repression of myelin gene expression.
Interpretation:
These studies suggest that NFIA participates in the control of oligodendrocyte progenitor differentiation and may contribute to the inhibition of remyelination in human myelin disorders. ANN NEUROL 2012;</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22807310</pmid><doi>10.1002/ana.23590</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenomatous Polyposis Coli Protein - metabolism Animals Arabidopsis Proteins - metabolism Biological and medical sciences Cell Differentiation - drug effects Cells, Cultured Cerebral Cortex - cytology Chromatin Immunoprecipitation Disease Models, Animal DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Electroporation Embryo, Mammalian Gene expression Gene Expression Regulation, Developmental - genetics Gene Expression Regulation, Developmental - physiology Homeodomain Proteins - metabolism Humans Hypoxia-Ischemia, Brain - metabolism Infant Infant, Newborn Injuries of the nervous system and the skull. Diseases due to physical agents Intramolecular Transferases - metabolism Leukoencephalopathies - chemically induced Leukoencephalopathies - metabolism Leukoencephalopathies - pathology Lysophosphatidylcholines - toxicity Medical research Medical sciences Mice Mice, Transgenic Multiple Sclerosis - metabolism Myelin Basic Protein - metabolism Neurology NFI Transcription Factors - genetics NFI Transcription Factors - metabolism Oligodendroglia - drug effects Oligodendroglia - metabolism Rodents Spinal Cord - pathology Stem Cells - drug effects Stem Cells - metabolism Time Factors Transcription Factors - genetics Transcription Factors - metabolism Traumas. Diseases due to physical agents |
| title | Evidence that nuclear factor IA inhibits repair after white matter injury |
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