Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease
Altered expression levels of protein-coding genes and microRNAs have been implicated in the pathogenesis of Huntington's disease (HD). The involvement of other ncRNAs, especially long ncRNAs (lncRNA), is being realized recently and the related knowledge is still rudimentary. Using small RNA seq...
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| Veröffentlicht in: | RNA biology 2018-10, Vol.15 (10), p.1348-1363 |
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| creator | Chanda, Kaushik Das, Srijit Chakraborty, Joyeeta Bucha, Sudha Maitra, Arindam Chatterjee, Raghunath Mukhopadhyay, Debashis Bhattacharyya, Nitai P |
| description | Altered expression levels of protein-coding genes and microRNAs have been implicated in the pathogenesis of Huntington's disease (HD). The involvement of other ncRNAs, especially long ncRNAs (lncRNA), is being realized recently and the related knowledge is still rudimentary. Using small RNA sequencing and PCR arrays we observed perturbations in the levels of 12 ncRNAs in HD mouse brain, eight of which had human homologs. Of these, Meg3, Neat1, and Xist showed a consistent and significant increase in HD cell and animal models. Transient knock-down of Meg3 and Neat1 in cell models of HD led to a significant decrease of aggregates formed by mutant huntingtin and downregulation of the endogenous Tp53 expression. Understanding Meg3 and Neat1 functions in the context of HD pathogenesis is likely to open up new strategies to control the disease. |
| doi_str_mv | 10.1080/15476286.2018.1534524 |
| format | Article |
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The involvement of other ncRNAs, especially long ncRNAs (lncRNA), is being realized recently and the related knowledge is still rudimentary. Using small RNA sequencing and PCR arrays we observed perturbations in the levels of 12 ncRNAs in HD mouse brain, eight of which had human homologs. Of these, Meg3, Neat1, and Xist showed a consistent and significant increase in HD cell and animal models. Transient knock-down of Meg3 and Neat1 in cell models of HD led to a significant decrease of aggregates formed by mutant huntingtin and downregulation of the endogenous Tp53 expression. Understanding Meg3 and Neat1 functions in the context of HD pathogenesis is likely to open up new strategies to control the disease.</description><identifier>ISSN: 1547-6286</identifier><identifier>EISSN: 1555-8584</identifier><identifier>DOI: 10.1080/15476286.2018.1534524</identifier><identifier>PMID: 30321100</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; Brain - metabolism ; Brain - pathology ; Disease Models, Animal ; Gene Expression Regulation - genetics ; Gene Knockdown Techniques ; Humans ; Huntingtin Protein - genetics ; Huntington Disease - genetics ; Huntington Disease - metabolism ; Huntington Disease - pathology ; Huntington's disease ; long ncRNA ; MEG3 ; Mice ; NEAT1 ; Research Paper ; RNA, Long Noncoding - antagonists & inhibitors ; RNA, Long Noncoding - genetics ; Sequence Analysis, RNA ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>RNA biology, 2018-10, Vol.15 (10), p.1348-1363</ispartof><rights>2018 Informa UK Limited, trading as Taylor & Francis Group 2018</rights><rights>2018 Informa UK Limited, trading as Taylor & Francis Group 2018 Informa UK Limited, trading as Taylor & Francis Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-16fd5edecbdbdceb7989d30b382fc7877ad40c338849f2439f11024edf00f0083</citedby><cites>FETCH-LOGICAL-c468t-16fd5edecbdbdceb7989d30b382fc7877ad40c338849f2439f11024edf00f0083</cites><orcidid>0000-0002-8600-5210 ; 0000-0003-4013-5615 ; 0000-0002-2531-9662 ; 0000-0002-4516-2260</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284602/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284602/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30321100$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chanda, Kaushik</creatorcontrib><creatorcontrib>Das, Srijit</creatorcontrib><creatorcontrib>Chakraborty, Joyeeta</creatorcontrib><creatorcontrib>Bucha, Sudha</creatorcontrib><creatorcontrib>Maitra, Arindam</creatorcontrib><creatorcontrib>Chatterjee, Raghunath</creatorcontrib><creatorcontrib>Mukhopadhyay, Debashis</creatorcontrib><creatorcontrib>Bhattacharyya, Nitai P</creatorcontrib><title>Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease</title><title>RNA biology</title><addtitle>RNA Biol</addtitle><description>Altered expression levels of protein-coding genes and microRNAs have been implicated in the pathogenesis of Huntington's disease (HD). The involvement of other ncRNAs, especially long ncRNAs (lncRNA), is being realized recently and the related knowledge is still rudimentary. Using small RNA sequencing and PCR arrays we observed perturbations in the levels of 12 ncRNAs in HD mouse brain, eight of which had human homologs. Of these, Meg3, Neat1, and Xist showed a consistent and significant increase in HD cell and animal models. Transient knock-down of Meg3 and Neat1 in cell models of HD led to a significant decrease of aggregates formed by mutant huntingtin and downregulation of the endogenous Tp53 expression. Understanding Meg3 and Neat1 functions in the context of HD pathogenesis is likely to open up new strategies to control the disease.</description><subject>Animals</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Disease Models, Animal</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Huntingtin Protein - genetics</subject><subject>Huntington Disease - genetics</subject><subject>Huntington Disease - metabolism</subject><subject>Huntington Disease - pathology</subject><subject>Huntington's disease</subject><subject>long ncRNA</subject><subject>MEG3</subject><subject>Mice</subject><subject>NEAT1</subject><subject>Research Paper</subject><subject>RNA, Long Noncoding - antagonists & inhibitors</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Sequence Analysis, RNA</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>1547-6286</issn><issn>1555-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UdtqFDEYDqLYuvoISu70ZrY5zmRuxGE9tLDdguitIZPDGskmbTJb6dubYbfF3hQCCX--U_IB8BajJUYCnWHOupaIdkkQFkvMKeOEPQOnmHPeCC7Y8_nMumYGnYBXpfxBiLai5y_BCUWUYIzQKfg1hMlma-Da3tpQYHJwneIWbvT3zVDgpd1SqKKBG6smDH2EKxsCHOpkiH6nArxMZuZdOXi-j5OP2ynF9wV-9sWqYl-DF06FYt8c9wX4-fXLj9V5s776drEa1o1mrZga3DrDrbF6NKPRdux60RuKRiqI053oOmUY0pQKwXpHGO1dTU-YNQ6hugRdgI8H3ev9uLNVIk5ZBXmda8Z8J5Py8vFN9L_lNt3K-jusRaQKfDgK5HSzt2WSO190fauKNu2LJJigjiNSzReAH6A6p1KydQ82GMm5G3nfjZy7kcduKu_d_xkfWPdlVMCnA8BHl_JO_U05GDmpu5CyyypqXyR92uMfzkydFg</recordid><startdate>20181003</startdate><enddate>20181003</enddate><creator>Chanda, Kaushik</creator><creator>Das, Srijit</creator><creator>Chakraborty, Joyeeta</creator><creator>Bucha, Sudha</creator><creator>Maitra, Arindam</creator><creator>Chatterjee, Raghunath</creator><creator>Mukhopadhyay, Debashis</creator><creator>Bhattacharyya, Nitai P</creator><general>Taylor & Francis</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8600-5210</orcidid><orcidid>https://orcid.org/0000-0003-4013-5615</orcidid><orcidid>https://orcid.org/0000-0002-2531-9662</orcidid><orcidid>https://orcid.org/0000-0002-4516-2260</orcidid></search><sort><creationdate>20181003</creationdate><title>Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease</title><author>Chanda, Kaushik ; Das, Srijit ; Chakraborty, Joyeeta ; Bucha, Sudha ; Maitra, Arindam ; Chatterjee, Raghunath ; Mukhopadhyay, Debashis ; Bhattacharyya, Nitai P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-16fd5edecbdbdceb7989d30b382fc7877ad40c338849f2439f11024edf00f0083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Disease Models, Animal</topic><topic>Gene Expression Regulation - genetics</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Huntingtin Protein - genetics</topic><topic>Huntington Disease - genetics</topic><topic>Huntington Disease - metabolism</topic><topic>Huntington Disease - pathology</topic><topic>Huntington's disease</topic><topic>long ncRNA</topic><topic>MEG3</topic><topic>Mice</topic><topic>NEAT1</topic><topic>Research Paper</topic><topic>RNA, Long Noncoding - antagonists & inhibitors</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Sequence Analysis, RNA</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chanda, Kaushik</creatorcontrib><creatorcontrib>Das, Srijit</creatorcontrib><creatorcontrib>Chakraborty, Joyeeta</creatorcontrib><creatorcontrib>Bucha, Sudha</creatorcontrib><creatorcontrib>Maitra, Arindam</creatorcontrib><creatorcontrib>Chatterjee, Raghunath</creatorcontrib><creatorcontrib>Mukhopadhyay, Debashis</creatorcontrib><creatorcontrib>Bhattacharyya, Nitai P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>RNA biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chanda, Kaushik</au><au>Das, Srijit</au><au>Chakraborty, Joyeeta</au><au>Bucha, Sudha</au><au>Maitra, Arindam</au><au>Chatterjee, Raghunath</au><au>Mukhopadhyay, Debashis</au><au>Bhattacharyya, Nitai P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease</atitle><jtitle>RNA biology</jtitle><addtitle>RNA Biol</addtitle><date>2018-10-03</date><risdate>2018</risdate><volume>15</volume><issue>10</issue><spage>1348</spage><epage>1363</epage><pages>1348-1363</pages><issn>1547-6286</issn><eissn>1555-8584</eissn><abstract>Altered expression levels of protein-coding genes and microRNAs have been implicated in the pathogenesis of Huntington's disease (HD). 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| subjects | Animals Brain - metabolism Brain - pathology Disease Models, Animal Gene Expression Regulation - genetics Gene Knockdown Techniques Humans Huntingtin Protein - genetics Huntington Disease - genetics Huntington Disease - metabolism Huntington Disease - pathology Huntington's disease long ncRNA MEG3 Mice NEAT1 Research Paper RNA, Long Noncoding - antagonists & inhibitors RNA, Long Noncoding - genetics Sequence Analysis, RNA Tumor Suppressor Protein p53 - genetics |
| title | Altered Levels of Long NcRNAs Meg3 and Neat1 in Cell And Animal Models Of Huntington's Disease |
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