Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease
Huntington’s disease (HD) is a devastating neurodegenerative disease caused by cytosine-adenine-guanine trinucleotide repeat expansion in the huntingtin gene. Growing evidence supports the regulatory functions of long noncoding RNAs (lncRNAs) in the disease process, but little is known about the ass...
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| Veröffentlicht in: | Molecular neurobiology 2017-03, Vol.54 (2), p.1577-1586 |
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| creator | Sunwoo, Jun-Sang Lee, Soon-Tae Im, Wooseok Lee, Mijung Byun, Jung-Ick Jung, Keun-Hwa Park, Kyung-Il Jung, Ki-Young Lee, Sang Kun Chu, Kon Kim, Manho |
| description | Huntington’s disease (HD) is a devastating neurodegenerative disease caused by cytosine-adenine-guanine trinucleotide repeat expansion in the huntingtin gene. Growing evidence supports the regulatory functions of long noncoding RNAs (lncRNAs) in the disease process, but little is known about the association between lncRNAs and neuronal death in HD. Here, we evaluated the altered expression profiles of lncRNA in HD by using microarrays. Among dysregulated lncRNAs, we focused on the upregulation of nuclear paraspeckle assembly transcript 1 (NEAT1). Quantitative PCR analysis validated increased NEAT1 levels in the R6/2 mouse brain as well as the human HD postmortem brain. To determine the biological effects of NEAT1 on neuronal survival, neuro2A cells were transfected with the NEAT1 short isoform vector and were subjected to H
2
O
2
-induced injury. Subsequently, NEAT1-transfected cells showed increased viability under oxidative stress. Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD. |
| doi_str_mv | 10.1007/s12035-016-9928-9 |
| format | Article |
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2
O
2
-induced injury. Subsequently, NEAT1-transfected cells showed increased viability under oxidative stress. Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-016-9928-9</identifier><identifier>PMID: 27221610</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Tumor ; Female ; Gene Expression ; Humans ; Huntington Disease - genetics ; Huntington Disease - metabolism ; Huntington Disease - pathology ; Huntingtons disease ; Male ; Mice, Inbred CBA ; Mice, Transgenic ; Middle Aged ; Neurobiology ; Neurology ; Neurosciences ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - biosynthesis ; RNA, Long Noncoding - genetics</subject><ispartof>Molecular neurobiology, 2017-03, Vol.54 (2), p.1577-1586</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>Molecular Neurobiology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-483b4587f65aecb66735f0820c8243ebb1639d27e9286abc7b4db96b5f20c8e3</citedby><cites>FETCH-LOGICAL-c471t-483b4587f65aecb66735f0820c8243ebb1639d27e9286abc7b4db96b5f20c8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-016-9928-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-016-9928-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27221610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sunwoo, Jun-Sang</creatorcontrib><creatorcontrib>Lee, Soon-Tae</creatorcontrib><creatorcontrib>Im, Wooseok</creatorcontrib><creatorcontrib>Lee, Mijung</creatorcontrib><creatorcontrib>Byun, Jung-Ick</creatorcontrib><creatorcontrib>Jung, Keun-Hwa</creatorcontrib><creatorcontrib>Park, Kyung-Il</creatorcontrib><creatorcontrib>Jung, Ki-Young</creatorcontrib><creatorcontrib>Lee, Sang Kun</creatorcontrib><creatorcontrib>Chu, Kon</creatorcontrib><creatorcontrib>Kim, Manho</creatorcontrib><title>Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Huntington’s disease (HD) is a devastating neurodegenerative disease caused by cytosine-adenine-guanine trinucleotide repeat expansion in the huntingtin gene. Growing evidence supports the regulatory functions of long noncoding RNAs (lncRNAs) in the disease process, but little is known about the association between lncRNAs and neuronal death in HD. Here, we evaluated the altered expression profiles of lncRNA in HD by using microarrays. Among dysregulated lncRNAs, we focused on the upregulation of nuclear paraspeckle assembly transcript 1 (NEAT1). Quantitative PCR analysis validated increased NEAT1 levels in the R6/2 mouse brain as well as the human HD postmortem brain. To determine the biological effects of NEAT1 on neuronal survival, neuro2A cells were transfected with the NEAT1 short isoform vector and were subjected to H
2
O
2
-induced injury. Subsequently, NEAT1-transfected cells showed increased viability under oxidative stress. Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Huntington Disease - genetics</subject><subject>Huntington Disease - metabolism</subject><subject>Huntington Disease - pathology</subject><subject>Huntingtons disease</subject><subject>Male</subject><subject>Mice, Inbred CBA</subject><subject>Mice, Transgenic</subject><subject>Middle Aged</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - biosynthesis</subject><subject>RNA, Long Noncoding - genetics</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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><recordid>eNqFkc9qGzEQh0VJady0D5BLEOTSy7Yarf4eTeI2BeNC8V2sdmeTDbbkSLuQ3PIaeb0-SWWclhIIPWnQfPMbho-QU2CfgTH9JQNntawYqMpabir7hsxASlsBGH5EZszYutJKmGPyPudbxjgHpt-RY65LpYDNyHK-GTFhRxf3u4Q5DzHQ2NPxBukyhmu6iqGN3VCqn6s5XS3ma6BDoFdTGMvnGMOvx6dML4eMTcYP5G3fbDJ-fH5PyPrrYn1xVS1_fPt-MV9WrdAwVsLUXkijeyUbbL1SupY9M5y1hosavQdV245rLDepxrfai85b5WW_R7A-IZ8OsbsU7ybMo9sOucXNpgkYp-zAaG0kq0vM_1GulLECbEHPX6C3cUqh3FEoZaQQAnih4EC1KeacsHe7NGyb9OCAub0Ud5DiihS3l-L2yWfPyZPfYvd34o-FAvADkEsrXGP6Z_Wrqb8BFX-U_Q</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Sunwoo, Jun-Sang</creator><creator>Lee, Soon-Tae</creator><creator>Im, Wooseok</creator><creator>Lee, Mijung</creator><creator>Byun, Jung-Ick</creator><creator>Jung, Keun-Hwa</creator><creator>Park, Kyung-Il</creator><creator>Jung, Ki-Young</creator><creator>Lee, Sang Kun</creator><creator>Chu, Kon</creator><creator>Kim, Manho</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20170301</creationdate><title>Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease</title><author>Sunwoo, Jun-Sang ; Lee, Soon-Tae ; Im, Wooseok ; Lee, Mijung ; Byun, Jung-Ick ; Jung, Keun-Hwa ; Park, Kyung-Il ; Jung, Ki-Young ; Lee, Sang Kun ; Chu, Kon ; Kim, Manho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-483b4587f65aecb66735f0820c8243ebb1639d27e9286abc7b4db96b5f20c8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Huntington Disease - 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Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sunwoo, Jun-Sang</au><au>Lee, Soon-Tae</au><au>Im, Wooseok</au><au>Lee, Mijung</au><au>Byun, Jung-Ick</au><au>Jung, Keun-Hwa</au><au>Park, Kyung-Il</au><au>Jung, Ki-Young</au><au>Lee, Sang Kun</au><au>Chu, Kon</au><au>Kim, Manho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>54</volume><issue>2</issue><spage>1577</spage><epage>1586</epage><pages>1577-1586</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Huntington’s disease (HD) is a devastating neurodegenerative disease caused by cytosine-adenine-guanine trinucleotide repeat expansion in the huntingtin gene. Growing evidence supports the regulatory functions of long noncoding RNAs (lncRNAs) in the disease process, but little is known about the association between lncRNAs and neuronal death in HD. Here, we evaluated the altered expression profiles of lncRNA in HD by using microarrays. Among dysregulated lncRNAs, we focused on the upregulation of nuclear paraspeckle assembly transcript 1 (NEAT1). Quantitative PCR analysis validated increased NEAT1 levels in the R6/2 mouse brain as well as the human HD postmortem brain. To determine the biological effects of NEAT1 on neuronal survival, neuro2A cells were transfected with the NEAT1 short isoform vector and were subjected to H
2
O
2
-induced injury. Subsequently, NEAT1-transfected cells showed increased viability under oxidative stress. Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27221610</pmid><doi>10.1007/s12035-016-9928-9</doi><tpages>10</tpages></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Tumor Female Gene Expression Humans Huntington Disease - genetics Huntington Disease - metabolism Huntington Disease - pathology Huntingtons disease Male Mice, Inbred CBA Mice, Transgenic Middle Aged Neurobiology Neurology Neurosciences Ribonucleic acid RNA RNA, Long Noncoding - biosynthesis RNA, Long Noncoding - genetics |
| title | Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease |
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