Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients

<p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Angelini Corrado [verfasserIn] Loro Emanuele [verfasserIn] Viola Antonella [verfasserIn] Lepore Saverio M [verfasserIn] Rinaldi Fabrizio [verfasserIn] Gambardella Stefano [verfasserIn] Vergani Lodovica [verfasserIn] Novelli Giuseppe [verfasserIn] Botta Annalisa [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Übergeordnetes Werk:	In: Journal of Translational Medicine - BMC, 2003, 8(2010), 1, p 48
Übergeordnetes Werk:	volume:8 ; year:2010 ; number:1, p 48

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1479-5876-8-48

Katalog-ID:	DOAJ022952535

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allfields	10.1186/1479-5876-8-48 doi (DE-627)DOAJ022952535 (DE-599)DOAJ13572573806e427ab5d09811a2801e8f DE-627 ger DE-627 rakwb eng Angelini Corrado verfasserin aut Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Medicine R Loro Emanuele verfasserin aut Viola Antonella verfasserin aut Lepore Saverio M verfasserin aut Rinaldi Fabrizio verfasserin aut Gambardella Stefano verfasserin aut Vergani Lodovica verfasserin aut Novelli Giuseppe verfasserin aut Botta Annalisa verfasserin aut In Journal of Translational Medicine BMC, 2003 8(2010), 1, p 48 (DE-627)369084136 (DE-600)2118570-0 14795876 nnns volume:8 year:2010 number:1, p 48 https://doi.org/10.1186/1479-5876-8-48 kostenfrei https://doaj.org/article/13572573806e427ab5d09811a2801e8f kostenfrei http://www.translational-medicine.com/content/8/1/48 kostenfrei https://doaj.org/toc/1479-5876 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1, p 48
spelling	10.1186/1479-5876-8-48 doi (DE-627)DOAJ022952535 (DE-599)DOAJ13572573806e427ab5d09811a2801e8f DE-627 ger DE-627 rakwb eng Angelini Corrado verfasserin aut Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Medicine R Loro Emanuele verfasserin aut Viola Antonella verfasserin aut Lepore Saverio M verfasserin aut Rinaldi Fabrizio verfasserin aut Gambardella Stefano verfasserin aut Vergani Lodovica verfasserin aut Novelli Giuseppe verfasserin aut Botta Annalisa verfasserin aut In Journal of Translational Medicine BMC, 2003 8(2010), 1, p 48 (DE-627)369084136 (DE-600)2118570-0 14795876 nnns volume:8 year:2010 number:1, p 48 https://doi.org/10.1186/1479-5876-8-48 kostenfrei https://doaj.org/article/13572573806e427ab5d09811a2801e8f kostenfrei http://www.translational-medicine.com/content/8/1/48 kostenfrei https://doaj.org/toc/1479-5876 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1, p 48
allfields_unstemmed	10.1186/1479-5876-8-48 doi (DE-627)DOAJ022952535 (DE-599)DOAJ13572573806e427ab5d09811a2801e8f DE-627 ger DE-627 rakwb eng Angelini Corrado verfasserin aut Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Medicine R Loro Emanuele verfasserin aut Viola Antonella verfasserin aut Lepore Saverio M verfasserin aut Rinaldi Fabrizio verfasserin aut Gambardella Stefano verfasserin aut Vergani Lodovica verfasserin aut Novelli Giuseppe verfasserin aut Botta Annalisa verfasserin aut In Journal of Translational Medicine BMC, 2003 8(2010), 1, p 48 (DE-627)369084136 (DE-600)2118570-0 14795876 nnns volume:8 year:2010 number:1, p 48 https://doi.org/10.1186/1479-5876-8-48 kostenfrei https://doaj.org/article/13572573806e427ab5d09811a2801e8f kostenfrei http://www.translational-medicine.com/content/8/1/48 kostenfrei https://doaj.org/toc/1479-5876 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1, p 48
allfieldsGer	10.1186/1479-5876-8-48 doi (DE-627)DOAJ022952535 (DE-599)DOAJ13572573806e427ab5d09811a2801e8f DE-627 ger DE-627 rakwb eng Angelini Corrado verfasserin aut Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Medicine R Loro Emanuele verfasserin aut Viola Antonella verfasserin aut Lepore Saverio M verfasserin aut Rinaldi Fabrizio verfasserin aut Gambardella Stefano verfasserin aut Vergani Lodovica verfasserin aut Novelli Giuseppe verfasserin aut Botta Annalisa verfasserin aut In Journal of Translational Medicine BMC, 2003 8(2010), 1, p 48 (DE-627)369084136 (DE-600)2118570-0 14795876 nnns volume:8 year:2010 number:1, p 48 https://doi.org/10.1186/1479-5876-8-48 kostenfrei https://doaj.org/article/13572573806e427ab5d09811a2801e8f kostenfrei http://www.translational-medicine.com/content/8/1/48 kostenfrei https://doaj.org/toc/1479-5876 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1, p 48
allfieldsSound	10.1186/1479-5876-8-48 doi (DE-627)DOAJ022952535 (DE-599)DOAJ13572573806e427ab5d09811a2801e8f DE-627 ger DE-627 rakwb eng Angelini Corrado verfasserin aut Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p< Medicine R Loro Emanuele verfasserin aut Viola Antonella verfasserin aut Lepore Saverio M verfasserin aut Rinaldi Fabrizio verfasserin aut Gambardella Stefano verfasserin aut Vergani Lodovica verfasserin aut Novelli Giuseppe verfasserin aut Botta Annalisa verfasserin aut In Journal of Translational Medicine BMC, 2003 8(2010), 1, p 48 (DE-627)369084136 (DE-600)2118570-0 14795876 nnns volume:8 year:2010 number:1, p 48 https://doi.org/10.1186/1479-5876-8-48 kostenfrei https://doaj.org/article/13572573806e427ab5d09811a2801e8f kostenfrei http://www.translational-medicine.com/content/8/1/48 kostenfrei https://doaj.org/toc/1479-5876 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2010 1, p 48
language	English
source	In Journal of Translational Medicine 8(2010), 1, p 48 volume:8 year:2010 number:1, p 48
sourceStr	In Journal of Translational Medicine 8(2010), 1, p 48 volume:8 year:2010 number:1, p 48
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Medicine R
isfreeaccess_bool	true
container_title	Journal of Translational Medicine
authorswithroles_txt_mv	Angelini Corrado @@aut@@ Loro Emanuele @@aut@@ Viola Antonella @@aut@@ Lepore Saverio M @@aut@@ Rinaldi Fabrizio @@aut@@ Gambardella Stefano @@aut@@ Vergani Lodovica @@aut@@ Novelli Giuseppe @@aut@@ Botta Annalisa @@aut@@
publishDateDaySort_date	2010-01-01T00:00:00Z
hierarchy_top_id	369084136
id	DOAJ022952535
language_de	englisch
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They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. 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author	Angelini Corrado
spellingShingle	Angelini Corrado misc Medicine misc R Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
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topic_title	Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
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title	Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
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title_full	Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
author_sort	Angelini Corrado
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author_browse	Angelini Corrado Loro Emanuele Viola Antonella Lepore Saverio M Rinaldi Fabrizio Gambardella Stefano Vergani Lodovica Novelli Giuseppe Botta Annalisa
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author-letter	Angelini Corrado
doi_str_mv	10.1186/1479-5876-8-48
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title_sort	overexpression of microrna-206 in the skeletal muscle from myotonic dystrophy type 1 patients
title_auth	Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
abstract	<p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<MicroRNAs are highly conserved, noncoding RNAs involved in post-transcriptional gene silencing. They have been shown to participate in a wide range of biological processes, including myogenesis and muscle regeneration. The goal of this study is to test the hypothesis that myo-miRs (myo = muscle + miR = miRNA) expression is altered in muscle from patients affected by myotonic dystrophy type 1 (DM1), the most frequently inherited neuromuscular disease in adults. In order to gain better insights about the role of miRNAs in the DM1 pathogenesis, we have also analyzed the muscular expression of miR-103 and miR-107, which have been identified <it<in silico </it<as attractive candidates for binding to the <it<DMPK </it<mRNA.</p< <p<Methods</p< <p<To this aim, we have profiled the expression of miR-133 (miR-133a, miR-133b), miR-1, miR-181 (miR-181a, miR-181b, miR-181c) and miR-206, that are specifically induced during myogenesis in cardiac and skeletal muscle tissues. miR-103 and miR-107, highly expressed in brain, heart and muscle have also been included in this study. QRT-PCR experiments have been performed on RNA from vastus lateralis biopsies of DM1 patients (n = 7) and control subjects (n = 4). Results of miRNAs expression have been confirmed by Northern blot, whereas <it<in situ </it<hybridization technique have been performed to localize misexpressed miRNAs on muscle sections from DM1 and control individuals.</p< <p<Results</p< <p<Only miR-206 showed an over-expression in 5 of 7 DM1 patients (threshold = 2, fold change between 1.20 and 13.22, average = 5.37) compared to the control group. This result has been further confirmed by Northern blot analysis (3.37-fold overexpression, <it<R</it<<sup<2 </sup<= 0.89). <it<In situ </it<hybridization localized miR-206 to nuclear site both in normal and DM1 tissues. Cellular distribution in DM1 tissues includes also the nuclear regions of centralized nuclei, with a strong signal corresponding to nuclear clumps.</p< <p<Conclusions</p< <p<This work provides, for the first time, evidences about miRNAs misexpression in DM1 muscle tissues, adding a new element in the pathogenesis of this complex genetic disease.</p<
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title_short	Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients
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Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients

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