MicroRNA expression profiling in blood from fragile X‐associated tremor/ataxia syndrome patients
Fragile X‐associated tremor/ataxia syndrome (FXTAS) is a late‐onset neurodegenerative disorder associated with FMR1 gene premutation alleles (55–200 CGG repeats). Fragile X‐associated tremor/ataxia syndrome clinical core features include action tremor, gait ataxia, cognitive deficits progressing to...
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| Veröffentlicht in: | Genes, brain and behavior brain and behavior, 2013-08, Vol.12 (6), p.595-603 |
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| creator | Alvarez‐Mora, M. I. Rodriguez‐Revenga, L. Madrigal, I. Torres‐Silva, F. Mateu‐Huertas, E. Lizano, E. Friedländer, M. R. Martí, E. Estivill, X. Milà, M. |
| description | Fragile X‐associated tremor/ataxia syndrome (FXTAS) is a late‐onset neurodegenerative disorder associated with FMR1 gene premutation alleles (55–200 CGG repeats). Fragile X‐associated tremor/ataxia syndrome clinical core features include action tremor, gait ataxia, cognitive deficits progressing to dementia, and frequently parkinsonism. Although the pathogenic molecular mechanism of FXTAS is not completely understood, the restriction of the phenotype to the FMR1 premutation range has given rise to a model based on a RNA toxic gain‐of‐function. Since the identification of the first microRNAs (miRNAs) and their role in normal development, several studies have associated them with neurodegenerative diseases such as Parkinson, Alzheimer and Huntington diseases, suggesting that they play a key role in brain development, as well as in its morphogenesis. Herein, we present the characterization of miRNA expression profiles in FXTAS male patients using deep sequencing‐based technologies and microarray technology. Deep sequencing analysis evidenced 83 miRNAs that were significantly deregulated whereas microarray analysis showed 31. When comparing these results, 14 miRNAs were found deregulated in FXTAS patients. MiR‐424 and miR‐574‐3p showed significant fold change adjusted P‐values in both platforms in FXTAS patients. MiR‐424 has been founded substantially and specifically enriched in human cerebral cortical white matter of Alzheimer disease patients, which, together with cerebral atrophy, is a prominent imaging finding in individuals with FXTAS. The study provides the first systematic evidence of differential miRNA expression changes in FXTAS blood samples. Although further studies are necessary to better characterize the miRNA function in FXTAS disorder, our results suggest that they might contribute to its pathogenesis.
High‐throughput technologies have revealed 14 miRNAs deregulated in blood FXTAS samples relative to controls. |
| doi_str_mv | 10.1111/gbb.12061 |
| format | Article |
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High‐throughput technologies have revealed 14 miRNAs deregulated in blood FXTAS samples relative to controls.</description><identifier>ISSN: 1601-1848</identifier><identifier>EISSN: 1601-183X</identifier><identifier>DOI: 10.1111/gbb.12061</identifier><identifier>PMID: 23790110</identifier><identifier>CODEN: GBBEAO</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult and adolescent clinical studies ; Aged ; Ataxia ; Biological and medical sciences ; Blood ; Case-Control Studies ; Cerebellar Diseases - diagnosis ; Cerebellar Diseases - genetics ; Expression profile ; FMR1 gene ; Fragile X Mental Retardation Protein - genetics ; FXTAS ; Gene Expression Profiling ; Genes ; High-Throughput Nucleotide Sequencing ; high‐throughput technologies ; Humans ; IsomiR ; Male ; Medical sciences ; MicroRNAs - blood ; MicroRNAs - chemistry ; Middle Aged ; miRNAs ; mitochondrial dysfunction ; neurodegeneration ; Oligonucleotide Array Sequence Analysis ; Organic mental disorders. Neuropsychology ; oxidative stress ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Sequence Analysis, DNA ; trimming variants</subject><ispartof>Genes, brain and behavior, 2013-08, Vol.12 (6), p.595-603</ispartof><rights>2013 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society</rights><rights>2015 INIST-CNRS</rights><rights>2013 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4511-c5593ce54d8b8e4a830a3fd157176760993e23e4276ba4727fee28a64617eefb3</citedby><cites>FETCH-LOGICAL-c4511-c5593ce54d8b8e4a830a3fd157176760993e23e4276ba4727fee28a64617eefb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fgbb.12061$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fgbb.12061$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,11541,27901,27902,45550,45551,46027,46451</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fgbb.12061$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27649142$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23790110$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alvarez‐Mora, M. I.</creatorcontrib><creatorcontrib>Rodriguez‐Revenga, L.</creatorcontrib><creatorcontrib>Madrigal, I.</creatorcontrib><creatorcontrib>Torres‐Silva, F.</creatorcontrib><creatorcontrib>Mateu‐Huertas, E.</creatorcontrib><creatorcontrib>Lizano, E.</creatorcontrib><creatorcontrib>Friedländer, M. R.</creatorcontrib><creatorcontrib>Martí, E.</creatorcontrib><creatorcontrib>Estivill, X.</creatorcontrib><creatorcontrib>Milà, M.</creatorcontrib><title>MicroRNA expression profiling in blood from fragile X‐associated tremor/ataxia syndrome patients</title><title>Genes, brain and behavior</title><addtitle>Genes Brain Behav</addtitle><description>Fragile X‐associated tremor/ataxia syndrome (FXTAS) is a late‐onset neurodegenerative disorder associated with FMR1 gene premutation alleles (55–200 CGG repeats). Fragile X‐associated tremor/ataxia syndrome clinical core features include action tremor, gait ataxia, cognitive deficits progressing to dementia, and frequently parkinsonism. Although the pathogenic molecular mechanism of FXTAS is not completely understood, the restriction of the phenotype to the FMR1 premutation range has given rise to a model based on a RNA toxic gain‐of‐function. Since the identification of the first microRNAs (miRNAs) and their role in normal development, several studies have associated them with neurodegenerative diseases such as Parkinson, Alzheimer and Huntington diseases, suggesting that they play a key role in brain development, as well as in its morphogenesis. Herein, we present the characterization of miRNA expression profiles in FXTAS male patients using deep sequencing‐based technologies and microarray technology. Deep sequencing analysis evidenced 83 miRNAs that were significantly deregulated whereas microarray analysis showed 31. When comparing these results, 14 miRNAs were found deregulated in FXTAS patients. MiR‐424 and miR‐574‐3p showed significant fold change adjusted P‐values in both platforms in FXTAS patients. MiR‐424 has been founded substantially and specifically enriched in human cerebral cortical white matter of Alzheimer disease patients, which, together with cerebral atrophy, is a prominent imaging finding in individuals with FXTAS. The study provides the first systematic evidence of differential miRNA expression changes in FXTAS blood samples. Although further studies are necessary to better characterize the miRNA function in FXTAS disorder, our results suggest that they might contribute to its pathogenesis.
High‐throughput technologies have revealed 14 miRNAs deregulated in blood FXTAS samples relative to controls.</description><subject>Adult and adolescent clinical studies</subject><subject>Aged</subject><subject>Ataxia</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Case-Control Studies</subject><subject>Cerebellar Diseases - diagnosis</subject><subject>Cerebellar Diseases - genetics</subject><subject>Expression profile</subject><subject>FMR1 gene</subject><subject>Fragile X Mental Retardation Protein - genetics</subject><subject>FXTAS</subject><subject>Gene Expression Profiling</subject><subject>Genes</subject><subject>High-Throughput Nucleotide Sequencing</subject><subject>high‐throughput technologies</subject><subject>Humans</subject><subject>IsomiR</subject><subject>Male</subject><subject>Medical sciences</subject><subject>MicroRNAs - blood</subject><subject>MicroRNAs - chemistry</subject><subject>Middle Aged</subject><subject>miRNAs</subject><subject>mitochondrial dysfunction</subject><subject>neurodegeneration</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>oxidative stress</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Sequence Analysis, DNA</subject><subject>trimming variants</subject><issn>1601-1848</issn><issn>1601-183X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0UFr2zAUB3BRNpo27WFfYAhKYT2k0bNsyT4mYesGaQulhd6MbD8HFdvKJIc1t32EfsZ9kr4saQeFwnSQdPjpSU9_xj6BOAca40VRnEMkFOyxA1ACRpDK-w-v-zgdsMMQHoQALVPYZ4NI6kwAiANWXNrSu5urCcfHpccQrOv40rvaNrZbcNvxonGu4rV3LU1mYRvk939-P5kQXGlNjxXvPbbOj01vHq3hYd1VhJEvTW-x68MR-1ibJuDxbh2yu29fb2ffR_Prix-zyXxUxgnAqEySTJaYxFVapBibVAoj6woSDVppJbJMYiQxjrQqTKwjXSNGqVGxAo1YF3LIvmzr0vN_rjD0eWtDiU1jOnSrkAMdFSJSWvwHBZ1IGWWS6Mkb-uBWvqNGNirJUkWW1NlW0WeG4LHOl962xq9zEPkmo5wyyv9mRPbzruKqaLF6lS-hEDjdARNK09Cvd6UN_5xWcUbNkBtv3S8KZf3-jfnFdLq9-hlbk6eB</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Alvarez‐Mora, M. I.</creator><creator>Rodriguez‐Revenga, L.</creator><creator>Madrigal, I.</creator><creator>Torres‐Silva, F.</creator><creator>Mateu‐Huertas, E.</creator><creator>Lizano, E.</creator><creator>Friedländer, M. R.</creator><creator>Martí, E.</creator><creator>Estivill, X.</creator><creator>Milà, M.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>John Wiley & Sons, Inc</general><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>7QG</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>7TM</scope></search><sort><creationdate>201308</creationdate><title>MicroRNA expression profiling in blood from fragile X‐associated tremor/ataxia syndrome patients</title><author>Alvarez‐Mora, M. I. ; Rodriguez‐Revenga, L. ; Madrigal, I. ; Torres‐Silva, F. ; Mateu‐Huertas, E. ; Lizano, E. ; Friedländer, M. 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I.</au><au>Rodriguez‐Revenga, L.</au><au>Madrigal, I.</au><au>Torres‐Silva, F.</au><au>Mateu‐Huertas, E.</au><au>Lizano, E.</au><au>Friedländer, M. R.</au><au>Martí, E.</au><au>Estivill, X.</au><au>Milà, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA expression profiling in blood from fragile X‐associated tremor/ataxia syndrome patients</atitle><jtitle>Genes, brain and behavior</jtitle><addtitle>Genes Brain Behav</addtitle><date>2013-08</date><risdate>2013</risdate><volume>12</volume><issue>6</issue><spage>595</spage><epage>603</epage><pages>595-603</pages><issn>1601-1848</issn><eissn>1601-183X</eissn><coden>GBBEAO</coden><abstract>Fragile X‐associated tremor/ataxia syndrome (FXTAS) is a late‐onset neurodegenerative disorder associated with FMR1 gene premutation alleles (55–200 CGG repeats). Fragile X‐associated tremor/ataxia syndrome clinical core features include action tremor, gait ataxia, cognitive deficits progressing to dementia, and frequently parkinsonism. Although the pathogenic molecular mechanism of FXTAS is not completely understood, the restriction of the phenotype to the FMR1 premutation range has given rise to a model based on a RNA toxic gain‐of‐function. Since the identification of the first microRNAs (miRNAs) and their role in normal development, several studies have associated them with neurodegenerative diseases such as Parkinson, Alzheimer and Huntington diseases, suggesting that they play a key role in brain development, as well as in its morphogenesis. Herein, we present the characterization of miRNA expression profiles in FXTAS male patients using deep sequencing‐based technologies and microarray technology. Deep sequencing analysis evidenced 83 miRNAs that were significantly deregulated whereas microarray analysis showed 31. When comparing these results, 14 miRNAs were found deregulated in FXTAS patients. MiR‐424 and miR‐574‐3p showed significant fold change adjusted P‐values in both platforms in FXTAS patients. MiR‐424 has been founded substantially and specifically enriched in human cerebral cortical white matter of Alzheimer disease patients, which, together with cerebral atrophy, is a prominent imaging finding in individuals with FXTAS. The study provides the first systematic evidence of differential miRNA expression changes in FXTAS blood samples. Although further studies are necessary to better characterize the miRNA function in FXTAS disorder, our results suggest that they might contribute to its pathogenesis.
High‐throughput technologies have revealed 14 miRNAs deregulated in blood FXTAS samples relative to controls.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>23790110</pmid><doi>10.1111/gbb.12061</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult and adolescent clinical studies Aged Ataxia Biological and medical sciences Blood Case-Control Studies Cerebellar Diseases - diagnosis Cerebellar Diseases - genetics Expression profile FMR1 gene Fragile X Mental Retardation Protein - genetics FXTAS Gene Expression Profiling Genes High-Throughput Nucleotide Sequencing high‐throughput technologies Humans IsomiR Male Medical sciences MicroRNAs - blood MicroRNAs - chemistry Middle Aged miRNAs mitochondrial dysfunction neurodegeneration Oligonucleotide Array Sequence Analysis Organic mental disorders. Neuropsychology oxidative stress Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Sequence Analysis, DNA trimming variants |
| title | MicroRNA expression profiling in blood from fragile X‐associated tremor/ataxia syndrome patients |
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