The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses
High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific...
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| description | High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases. |
| doi_str_mv | 10.1371/journal.pone.0137637 |
| format | Article |
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However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0137637</identifier><identifier>PMID: 26376480</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptive systems ; Adhesive strength ; Agricultural biotechnology ; Analysis ; Animal models ; Animals ; Annotations ; Apoptosis ; Axonogenesis ; Biomarkers - metabolism ; Brain ; Care and treatment ; Cell adhesion ; Computational Biology - methods ; Corpus Striatum - cytology ; Corpus Striatum - metabolism ; Cytoskeleton ; Data processing ; Development and progression ; Disease Models, Animal ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genetic aspects ; Genetic engineering ; High-throughput screening ; Huntington Disease - genetics ; Huntington Disease - metabolism ; Huntington Disease - pathology ; Huntington's disease ; Huntingtons disease ; Immune system ; Medicine ; Mice ; Mice, Transgenic ; MicroRNA ; MicroRNAs - genetics ; miRNA ; Neostriatum ; Neurites - metabolism ; Neuroblastoma ; Neuroblastoma - genetics ; Neuroblastoma - pathology ; Neuroblastoma cells ; Neuroblasts ; Neurodegeneration ; Patient outcomes ; Phenotype ; Physiology ; Proteins ; Regulatory mechanisms (biology) ; Rodents ; Screening ; Signal transduction ; Transgenic animals ; Transgenic mice ; Wound healing</subject><ispartof>PloS one, 2015-09, Vol.10 (9), p.e0137637-e0137637</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Fu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Fu et al 2015 Fu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-5f08b53a69afc0747d8bfc0801963441bdb5a9dcb9a03e71014f296ef8c7f0ff3</citedby><cites>FETCH-LOGICAL-c692t-5f08b53a69afc0747d8bfc0801963441bdb5a9dcb9a03e71014f296ef8c7f0ff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574104/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574104/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79472,79473</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26376480$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zhang, Jianhua</contributor><creatorcontrib>Fu, Mu-Hui</creatorcontrib><creatorcontrib>Li, Chia-Ling</creatorcontrib><creatorcontrib>Lin, Hsiu-Lien</creatorcontrib><creatorcontrib>Tsai, Shaw-Jeng</creatorcontrib><creatorcontrib>Lai, Yen-Yu</creatorcontrib><creatorcontrib>Chang, Yu-Fan</creatorcontrib><creatorcontrib>Cheng, Pei-Hsun</creatorcontrib><creatorcontrib>Chen, Chuan-Mu</creatorcontrib><creatorcontrib>Yang, Shang-Hsun</creatorcontrib><title>The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases.</description><subject>Adaptive systems</subject><subject>Adhesive strength</subject><subject>Agricultural biotechnology</subject><subject>Analysis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Annotations</subject><subject>Apoptosis</subject><subject>Axonogenesis</subject><subject>Biomarkers - metabolism</subject><subject>Brain</subject><subject>Care and treatment</subject><subject>Cell adhesion</subject><subject>Computational Biology - methods</subject><subject>Corpus Striatum - cytology</subject><subject>Corpus Striatum - metabolism</subject><subject>Cytoskeleton</subject><subject>Data processing</subject><subject>Development and progression</subject><subject>Disease Models, Animal</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Genetic engineering</subject><subject>High-throughput screening</subject><subject>Huntington Disease - genetics</subject><subject>Huntington Disease - metabolism</subject><subject>Huntington Disease - pathology</subject><subject>Huntington's disease</subject><subject>Huntingtons disease</subject><subject>Immune system</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Neostriatum</subject><subject>Neurites - metabolism</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - genetics</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroblastoma cells</subject><subject>Neuroblasts</subject><subject>Neurodegeneration</subject><subject>Patient outcomes</subject><subject>Phenotype</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Regulatory mechanisms (biology)</subject><subject>Rodents</subject><subject>Screening</subject><subject>Signal transduction</subject><subject>Transgenic animals</subject><subject>Transgenic mice</subject><subject>Wound healing</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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><sourceid>DOA</sourceid><recordid>eNqNk01v1DAQhiMEoqXwDxBEqsTHYRc7dpz4grSUj65UVLQUrpbj2ImrxF5sB7H_HqebVhvUA8oh1viZ9x2PPUnyHIIlRAV8d20HZ3i33FojlyCGCCoeJMeQomxBMoAeHqyPkifeXwOQo5KQx8lRFlmCS3CcqKtWpt9skCZo3qUb2QwdD9bt0q9StNxo3_vUqrTXmwWkhKfapOdDhE0TrHnt04_aS-5lGlpnh6ZNP2irjbKu50GLdBUr3HnpnyaPFO-8fDb9T5Ifnz9dnZ0vLi6_rM9WFwtBaBYWuQJllSNOKFcCFLioyyouShCtEcawqquc01pUlAMkCwggVhklUpWiUEApdJK83OtuO-vZ1CLPYAFpVuZFmUVivSdqy6_Z1umeux2zXLObgHUN4y6W3klWYy6EwEQQxXEBaEVkhmlNZaYyVec0ar2f3Iaql7WITXS8m4nOd4xuWWN_M5wXGAIcBd5MAs7-GqQPrNdeyK7jRtrhpm5EMcR09Dr9B73_dBPV8HiA8SKirxhF2QpnZYkwRKPt8h4qfrXstYjvSekYnyW8nSVEJsg_oeGD92z9ffP_7OXPOfvqgG0l70LrbTcEbY2fg3gPCme9d1LdNRkCNo7DbTfYOA5sGoeY9uLwgu6Sbt8_-gtPJAWc</recordid><startdate>20150916</startdate><enddate>20150916</enddate><creator>Fu, Mu-Hui</creator><creator>Li, Chia-Ling</creator><creator>Lin, Hsiu-Lien</creator><creator>Tsai, Shaw-Jeng</creator><creator>Lai, Yen-Yu</creator><creator>Chang, Yu-Fan</creator><creator>Cheng, Pei-Hsun</creator><creator>Chen, Chuan-Mu</creator><creator>Yang, Shang-Hsun</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150916</creationdate><title>The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses</title><author>Fu, Mu-Hui ; Li, Chia-Ling ; Lin, Hsiu-Lien ; Tsai, Shaw-Jeng ; Lai, Yen-Yu ; Chang, Yu-Fan ; Cheng, Pei-Hsun ; Chen, Chuan-Mu ; Yang, Shang-Hsun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-5f08b53a69afc0747d8bfc0801963441bdb5a9dcb9a03e71014f296ef8c7f0ff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adaptive systems</topic><topic>Adhesive strength</topic><topic>Agricultural biotechnology</topic><topic>Analysis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Annotations</topic><topic>Apoptosis</topic><topic>Axonogenesis</topic><topic>Biomarkers - metabolism</topic><topic>Brain</topic><topic>Care and treatment</topic><topic>Cell adhesion</topic><topic>Computational Biology - methods</topic><topic>Corpus Striatum - cytology</topic><topic>Corpus Striatum - metabolism</topic><topic>Cytoskeleton</topic><topic>Data processing</topic><topic>Development and progression</topic><topic>Disease Models, Animal</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Genetic aspects</topic><topic>Genetic engineering</topic><topic>High-throughput screening</topic><topic>Huntington Disease - genetics</topic><topic>Huntington Disease - metabolism</topic><topic>Huntington Disease - pathology</topic><topic>Huntington's disease</topic><topic>Huntingtons disease</topic><topic>Immune system</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Neostriatum</topic><topic>Neurites - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fu, Mu-Hui</au><au>Li, Chia-Ling</au><au>Lin, Hsiu-Lien</au><au>Tsai, Shaw-Jeng</au><au>Lai, Yen-Yu</au><au>Chang, Yu-Fan</au><au>Cheng, Pei-Hsun</au><au>Chen, Chuan-Mu</au><au>Yang, Shang-Hsun</au><au>Zhang, Jianhua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-09-16</date><risdate>2015</risdate><volume>10</volume><issue>9</issue><spage>e0137637</spage><epage>e0137637</epage><pages>e0137637-e0137637</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26376480</pmid><doi>10.1371/journal.pone.0137637</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-09, Vol.10 (9), p.e0137637-e0137637 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1719285782 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adaptive systems Adhesive strength Agricultural biotechnology Analysis Animal models Animals Annotations Apoptosis Axonogenesis Biomarkers - metabolism Brain Care and treatment Cell adhesion Computational Biology - methods Corpus Striatum - cytology Corpus Striatum - metabolism Cytoskeleton Data processing Development and progression Disease Models, Animal Gene expression Gene Expression Profiling Gene Expression Regulation Genetic aspects Genetic engineering High-throughput screening Huntington Disease - genetics Huntington Disease - metabolism Huntington Disease - pathology Huntington's disease Huntingtons disease Immune system Medicine Mice Mice, Transgenic MicroRNA MicroRNAs - genetics miRNA Neostriatum Neurites - metabolism Neuroblastoma Neuroblastoma - genetics Neuroblastoma - pathology Neuroblastoma cells Neuroblasts Neurodegeneration Patient outcomes Phenotype Physiology Proteins Regulatory mechanisms (biology) Rodents Screening Signal transduction Transgenic animals Transgenic mice Wound healing |
| title | The Potential Regulatory Mechanisms of miR-196a in Huntington's Disease through Bioinformatic Analyses |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T05%3A09%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Potential%20Regulatory%20Mechanisms%20of%20miR-196a%20in%20Huntington's%20Disease%20through%20Bioinformatic%20Analyses&rft.jtitle=PloS%20one&rft.au=Fu,%20Mu-Hui&rft.date=2015-09-16&rft.volume=10&rft.issue=9&rft.spage=e0137637&rft.epage=e0137637&rft.pages=e0137637-e0137637&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0137637&rft_dat=%3Cgale_plos_%3EA428834134%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1719285782&rft_id=info:pmid/26376480&rft_galeid=A428834134&rft_doaj_id=oai_doaj_org_article_d4accc46c6fa4709b6e249d9e2f2fd59&rfr_iscdi=true |