Human endogenous retrovirus glycoprotein–mediated induction of redox reactants causes oligodendrocyte death and demyelination
Human endogenous retroviruses (HERVs) constitute 8% of the human genome and have been implicated in both health and disease. Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report tha...
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| Veröffentlicht in: | Nature neuroscience 2004-10, Vol.7 (10), p.1088-1095 |
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| creator | Antony, Joseph M van Marle, Guido Opii, Wycliffe Butterfield, D Allan Mallet, François Yong, Voon Wee Wallace, John L Deacon, Robert M Warren, Kenneth Power, Christopher |
| description | Human endogenous retroviruses (HERVs) constitute 8% of the human genome and have been implicated in both health and disease. Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report that the HERV-W encoded glycoprotein syncytin is upregulated in glial cells within acute demyelinating lesions of multiple sclerosis patients. Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. Thus, syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention. |
| doi_str_mv | 10.1038/nn1319 |
| format | Article |
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Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report that the HERV-W encoded glycoprotein syncytin is upregulated in glial cells within acute demyelinating lesions of multiple sclerosis patients. Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. Thus, syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention.</description><identifier>ISSN: 1097-6256</identifier><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/nn1319</identifier><identifier>PMID: 15452578</identifier><identifier>CODEN: NANEFN</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Adult ; Aged ; Animal Genetics and Genomics ; Animals ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Astrocytes - immunology ; Astrocytes - metabolism ; Astrocytes - virology ; Behavioral Sciences ; Biological Techniques ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Cell Death - immunology ; Cell Line ; Coumaric Acids - pharmacology ; Coumaric Acids - therapeutic use ; Demyelinating diseases ; Dendrites ; Diagnosis ; Disease ; Disease Models, Animal ; Encephalitis - drug therapy ; Encephalitis - immunology ; Encephalitis - virology ; Endogenous Retroviruses - genetics ; Endogenous Retroviruses - immunology ; Endogenous Retroviruses - metabolism ; Gene Products, env - genetics ; Gene Products, env - metabolism ; Genomes ; Glycoproteins ; Human endogenous retrovirus ; Humans ; Mice ; Middle Aged ; Multiple sclerosis ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - immunology ; Multiple Sclerosis - virology ; Myelin Sheath - metabolism ; Nervous system ; Neurobiology ; Neurosciences ; Nitric oxide ; Oligodendroglia - immunology ; Oligodendroglia - metabolism ; Oxidation-Reduction ; Physiological aspects ; Pregnancy Proteins - genetics ; Pregnancy Proteins - metabolism ; Proteins ; Rats ; Reactive Oxygen Species - antagonists & inhibitors ; Reactive Oxygen Species - metabolism ; Recombinant Fusion Proteins - pharmacology ; Risk factors ; RNA, Messenger - metabolism</subject><ispartof>Nature neuroscience, 2004-10, Vol.7 (10), p.1088-1095</ispartof><rights>Springer Nature America, Inc. 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Oct 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-faf834ddee12d7bc28d17a46c282e963948519aed90d626e6fa40c4284fe34aa3</citedby><cites>FETCH-LOGICAL-c440t-faf834ddee12d7bc28d17a46c282e963948519aed90d626e6fa40c4284fe34aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nn1319$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nn1319$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15452578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Antony, Joseph M</creatorcontrib><creatorcontrib>van Marle, Guido</creatorcontrib><creatorcontrib>Opii, Wycliffe</creatorcontrib><creatorcontrib>Butterfield, D Allan</creatorcontrib><creatorcontrib>Mallet, François</creatorcontrib><creatorcontrib>Yong, Voon Wee</creatorcontrib><creatorcontrib>Wallace, John L</creatorcontrib><creatorcontrib>Deacon, Robert M</creatorcontrib><creatorcontrib>Warren, Kenneth</creatorcontrib><creatorcontrib>Power, Christopher</creatorcontrib><title>Human endogenous retrovirus glycoprotein–mediated induction of redox reactants causes oligodendrocyte death and demyelination</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><addtitle>Nat Neurosci</addtitle><description>Human endogenous retroviruses (HERVs) constitute 8% of the human genome and have been implicated in both health and disease. Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report that the HERV-W encoded glycoprotein syncytin is upregulated in glial cells within acute demyelinating lesions of multiple sclerosis patients. Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. 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Academic</collection><jtitle>Nature neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Antony, Joseph M</au><au>van Marle, Guido</au><au>Opii, Wycliffe</au><au>Butterfield, D Allan</au><au>Mallet, François</au><au>Yong, Voon Wee</au><au>Wallace, John L</au><au>Deacon, Robert M</au><au>Warren, Kenneth</au><au>Power, Christopher</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human endogenous retrovirus glycoprotein–mediated induction of redox reactants causes oligodendrocyte death and demyelination</atitle><jtitle>Nature neuroscience</jtitle><stitle>Nat Neurosci</stitle><addtitle>Nat Neurosci</addtitle><date>2004-10-01</date><risdate>2004</risdate><volume>7</volume><issue>10</issue><spage>1088</spage><epage>1095</epage><pages>1088-1095</pages><issn>1097-6256</issn><eissn>1546-1726</eissn><coden>NANEFN</coden><abstract>Human endogenous retroviruses (HERVs) constitute 8% of the human genome and have been implicated in both health and disease. Increased HERV gene activity occurs in immunologically activated glia, although the consequences of HERV expression in the nervous system remain uncertain. Here, we report that the HERV-W encoded glycoprotein syncytin is upregulated in glial cells within acute demyelinating lesions of multiple sclerosis patients. Syncytin expression in astrocytes induced the release of redox reactants, which were cytotoxic to oligodendrocytes. Syncytin-mediated neuroinflammation and death of oligodendrocytes, with the ensuing neurobehavioral deficits, were prevented by the antioxidant ferulic acid in a mouse model of multiple sclerosis. Thus, syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15452578</pmid><doi>10.1038/nn1319</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Aged Animal Genetics and Genomics Animals Antioxidants - pharmacology Antioxidants - therapeutic use Astrocytes - immunology Astrocytes - metabolism Astrocytes - virology Behavioral Sciences Biological Techniques Biomedical and Life Sciences Biomedicine Brain Cell Death - immunology Cell Line Coumaric Acids - pharmacology Coumaric Acids - therapeutic use Demyelinating diseases Dendrites Diagnosis Disease Disease Models, Animal Encephalitis - drug therapy Encephalitis - immunology Encephalitis - virology Endogenous Retroviruses - genetics Endogenous Retroviruses - immunology Endogenous Retroviruses - metabolism Gene Products, env - genetics Gene Products, env - metabolism Genomes Glycoproteins Human endogenous retrovirus Humans Mice Middle Aged Multiple sclerosis Multiple Sclerosis - drug therapy Multiple Sclerosis - immunology Multiple Sclerosis - virology Myelin Sheath - metabolism Nervous system Neurobiology Neurosciences Nitric oxide Oligodendroglia - immunology Oligodendroglia - metabolism Oxidation-Reduction Physiological aspects Pregnancy Proteins - genetics Pregnancy Proteins - metabolism Proteins Rats Reactive Oxygen Species - antagonists & inhibitors Reactive Oxygen Species - metabolism Recombinant Fusion Proteins - pharmacology Risk factors RNA, Messenger - metabolism |
| title | Human endogenous retrovirus glycoprotein–mediated induction of redox reactants causes oligodendrocyte death and demyelination |
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