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  1. Article ; Online: MicroRNAs in skeletal muscle: their role and regulation in development, disease and function.

    Güller, Isabelle / Russell, Aaron P

    The Journal of physiology

    2010  Volume 588, Issue Pt 21, Page(s) 4075–4087

    Abstract: Maintaining skeletal muscle function throughout the lifespan is a prerequisite for good health and independent living. For skeletal muscle to consistently function at optimal levels, the efficient activation of processes that regulate muscle development, ...

    Abstract Maintaining skeletal muscle function throughout the lifespan is a prerequisite for good health and independent living. For skeletal muscle to consistently function at optimal levels, the efficient activation of processes that regulate muscle development, growth, regeneration and metabolism is required. Numerous conditions including neuromuscular disorders, physical inactivity, chronic disease and ageing are associated with perturbations in skeletal muscle function. A loss or reduction in skeletal muscle function often leads to increased morbidity and mortality either directly, or indirectly, via the development of secondary diseases such as diabetes, obesity, cardiovascular and respiratory disease. Identifying mechanisms which influence the processes regulating skeletal muscle function is a key priority. The discovery of microRNAs (miRNAs) provides a new avenue that will extend our knowledge of factors controlling skeletal muscle function. miRNAs may also improve our understanding and application of current therapeutic approaches as well as enable the identification of new therapeutic strategies and targets aimed at maintaining and/or improving skeletal muscle health. This review brings together the latest developments in skeletal muscle miRNA biology and focuses on their role and regulation under physiological and patho-physiological conditions with an emphasis on: myogenesis, hypertrophy, atrophy and regeneration; exercise and nutrition; muscle disease, ageing, diabetes and obesity.
    MeSH term(s) Aging/physiology ; Animals ; Diabetes Mellitus/physiopathology ; Exercise/physiology ; Humans ; MicroRNAs/physiology ; Muscle Development/physiology ; Muscle, Skeletal/physiology ; Muscle, Skeletal/physiopathology ; Musculoskeletal Diseases/physiopathology
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2010-08-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2010.194175
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Comparative analysis of microRNA expression in mouse and human brown adipose tissue.

    Güller, Isabelle / McNaughton, Sarah / Crowley, Tamsyn / Gilsanz, Vicente / Kajimura, Shingo / Watt, Matthew / Russell, Aaron P

    BMC genomics

    2015  Volume 16, Page(s) 820

    Abstract: Background: In small mammals brown adipose tissue (BAT) plays a predominant role in regulating energy expenditure (EE) via adaptive thermogenesis. New-born babies require BAT to control their body temperature, however its relevance in adults has been ... ...

    Abstract Background: In small mammals brown adipose tissue (BAT) plays a predominant role in regulating energy expenditure (EE) via adaptive thermogenesis. New-born babies require BAT to control their body temperature, however its relevance in adults has been questioned. Active BAT has recently been observed in adult humans, albeit in much lower relative quantities than small mammals. Comparing and contrasting the molecular mechanisms controlling BAT growth and development in mice and humans will increase our understanding or how human BAT is developed and may identify potential therapeutic targets to increase EE. MicroRNAs are molecular mechanisms involved in mouse BAT development however, little is known about the miRNA profile in human BAT. The aims of this study were to establish a mouse BAT-enriched miRNA profile and compare this with miRNAs measured in human BAT. To achieve this we firstly established a mouse BAT enriched-miRNA profile by comparing miRNAs expressed in mouse BAT, white adipose tissue and skeletal muscle. Following this the BAT-enriched miRNAs predicted to target genes potentially involved in growth and development were identified.
    Methods: MiRNA levels were measured using PCR-based miRNA arrays. Results were analysed using ExpressionSuite software with the global mean expression value of all expressed miRNAs in a givensample used as the normalisation factor. Bio-informatic analyses was used to predict gene targets followed by Ingenuity Pathway Analysis.
    Results: We identified 35 mouse BAT-enriched miRNAs that were predicted to target genes potentially involved in growth and development. We also identified 145 miRNAs expressed in both mouse and human BAT, of which 25 were enriched in mouse BAT. Of these 25 miRNAs, miR-20a was predicted to target MYF5 and PPARγ, two important genes involved in brown adipogenesis, as well as BMP2 and BMPR2, genes involved in white adipogenesis. For the first time, 69 miRNAs were identified in human BAT but absent in mouse BAT, and 181 miRNAs were expressed in mouse but not in human BAT.
    Conclusion: The present study has identified a small sub-set of miRNAs common to both mouse and human BAT. From this sub-set bioinformatics analysis suggested a potential role of miR-20a in the control of cell fate and this warrants further investigation. The large number of miRNAs found only in mouse BAT or only in human BAT highlights the differing molecular profile between species that is likely to influence the functional role of BAT across species. Nevertheless the BAT-enriched miRNA profiles established in the present study suggest targets to investigate in the control BAT development and EE.
    MeSH term(s) Adipogenesis/genetics ; Adipose Tissue, Brown ; Adult ; Animals ; Cell Differentiation/genetics ; Computational Biology ; Energy Metabolism/genetics ; Gene Expression Regulation, Developmental ; Humans ; Mice ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Oligonucleotide Array Sequence Analysis ; Thermogenesis/genetics
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2015-10-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/s12864-015-2045-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Regulation of miRNAs in human skeletal muscle following acute endurance exercise and short-term endurance training.

    Russell, Aaron P / Lamon, Severine / Boon, Hanneke / Wada, Shogo / Güller, Isabelle / Brown, Erin L / Chibalin, Alexander V / Zierath, Juleen R / Snow, Rod J / Stepto, Nigel / Wadley, Glenn D / Akimoto, Takayuki

    The Journal of physiology

    2013  Volume 591, Issue 18, Page(s) 4637–4653

    Abstract: The identification of microRNAs (miRNAs) has established new mechanisms that control skeletal muscle adaptation to exercise. The present study investigated the mRNA regulation of components of the miRNA biogenesis pathway (Drosha, Dicer and Exportin-5), ... ...

    Abstract The identification of microRNAs (miRNAs) has established new mechanisms that control skeletal muscle adaptation to exercise. The present study investigated the mRNA regulation of components of the miRNA biogenesis pathway (Drosha, Dicer and Exportin-5), muscle enriched miRNAs, (miR-1, -133a, -133b and -206), and several miRNAs dysregulated in muscle myopathies (miR-9, -23, -29, -31 and -181). Measurements were made in muscle biopsies from nine healthy untrained males at rest, 3 h following an acute bout of moderate-intensity endurance cycling and following 10 days of endurance training. Bioinformatics analysis was used to predict potential miRNA targets. In the 3 h period following the acute exercise bout, Drosha, Dicer and Exportin-5, as well as miR-1, -133a, -133-b and -181a were all increased. In contrast miR-9, -23a, -23b and -31 were decreased. Short-term training increased miR-1 and -29b, while miR-31 remained decreased. Negative correlations were observed between miR-9 and HDAC4 protein (r=-0.71; P=0.04), miR-31 and HDAC4 protein (r=-0.87; P=0.026) and miR-31 and NRF1 protein (r=-0.77; P=0.01) 3 h following exercise. miR-31 binding to the HDAC4 and NRF1 3 untranslated region (UTR) reduced luciferase reporter activity. Exercise rapidly and transiently regulates several miRNA species in muscle. Several of these miRNAs may be involved in the regulation of skeletal muscle regeneration, gene transcription and mitochondrial biogenesis. Identifying endurance exercise-mediated stress signals regulating skeletal muscle miRNAs, as well as validating their targets and regulatory pathways post exercise, will advance our understanding of their potential role/s in human health.
    MeSH term(s) Adult ; Computational Biology ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Exercise ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Karyopherins/genetics ; Karyopherins/metabolism ; Male ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiology ; Nuclear Respiratory Factor 1/genetics ; Nuclear Respiratory Factor 1/metabolism ; Physical Endurance ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Ribonuclease III/genetics ; Ribonuclease III/metabolism
    Chemical Substances Karyopherins ; MicroRNAs ; NRF1 protein, human ; Nuclear Respiratory Factor 1 ; Repressor Proteins ; XPO5 protein, human ; DICER1 protein, human (EC 3.1.26.3) ; DROSHA protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; HDAC4 protein, human (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2013-06-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2013.255695
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The microRNA signature in response to insulin reveals its implication in the transcriptional action of insulin in human skeletal muscle and the role of a sterol regulatory element-binding protein-1c/myocyte enhancer factor 2C pathway.

    Granjon, Aurélie / Gustin, Marie-Paule / Rieusset, Jennifer / Lefai, Etienne / Meugnier, Emmanuelle / Güller, Isabelle / Cerutti, Catherine / Paultre, Christian / Disse, Emmanuel / Rabasa-Lhoret, Rémi / Laville, Martine / Vidal, Hubert / Rome, Sophie

    Diabetes

    2009  Volume 58, Issue 11, Page(s) 2555–2564

    Abstract: Objective: Factors governing microRNA expressions in response to changes of cellular environment are still largely unknown. Our aim was to determine whether insulin, the major hormone controlling whole-body energy homeostasis, is involved in the ... ...

    Abstract Objective: Factors governing microRNA expressions in response to changes of cellular environment are still largely unknown. Our aim was to determine whether insulin, the major hormone controlling whole-body energy homeostasis, is involved in the regulation of microRNA expressions in human skeletal muscle.
    Research design and methods: We carried out comparative microRNA (miRNA) expression profiles in human skeletal muscle biopsies before and after a 3-h euglycemic-hyperinsulinemic clamp, with TaqMan low-density arrays. Then, using DNA microarrays, we determined the response to insulin of the miRNA putative target genes in order to determine their role in the transcriptional action of insulin. We further characterized the mechanism of action of insulin on two representative miRNAs, miR-1 and miR-133a, in human muscle cells.
    Results: Insulin downregulated the expressions of 39 distinct miRNAs in human skeletal muscle. Their potential target mRNAs coded for proteins that were mainly involved in insulin signaling and ubiquitination-mediated proteolysis. Bioinformatic analysis suggested that combinations of different downregulated miRNAs worked in concert to regulate gene expressions in response to insulin. We further demonstrated that sterol regulatory element-binding protein (SREBP)-1c and myocyte enhancer factor 2C were involved in the effect of insulin on miR-1 and miR-133a expression. Interestingly, we found an impaired regulation of miRNAs by insulin in the skeletal muscle of type 2 diabetic patients, likely as consequences of altered SREBP-1c activation.
    Conclusions: This work demonstrates a new role of insulin in the regulation of miRNAs in human skeletal muscle and suggests a possible implication of these new modulators in insulin resistance.
    MeSH term(s) Biopsy ; Cell Line ; DNA, Complementary/genetics ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/physiopathology ; Down-Regulation ; Gene Expression Regulation ; Glucose Clamp Technique ; Humans ; Hyperglycemia/physiopathology ; Hyperinsulinism/physiopathology ; Insulin/genetics ; MEF2 Transcription Factors ; MicroRNAs/genetics ; Muscle, Skeletal/physiology ; Myogenic Regulatory Factors/physiology ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction ; Reference Values ; Sterol Regulatory Element Binding Protein 1/genetics ; Sterol Regulatory Element Binding Protein 1/physiology ; Transcription, Genetic
    Chemical Substances DNA, Complementary ; Insulin ; MEF2 Transcription Factors ; MicroRNAs ; Myogenic Regulatory Factors ; Sterol Regulatory Element Binding Protein 1
    Language English
    Publishing date 2009-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db09-0165
    Database MEDical Literature Analysis and Retrieval System OnLINE

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