&lt;i&gt;MyoD&lt;/i&gt; is regulated by the miR-29a-&lt;i&gt;Tet1&lt;/i&gt; pathway in C2C12 myoblast cells

Chikenji, Akiyoshi; Ando, Hironori; Nariyama, Megumi; Suga, Takeo; Iida, Ryohei; Gomi, Kazuhiro

doi:10.2334/josnusd.15-0684

Cited by 8 publications

(10 citation statements)

References 37 publications

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“…Notably, we have considered only miR families conserved in mammals. Subsequently, we decided to address the miR‐29 family, the second top‐rated miR family previously described as being involved in skeletal muscle differentiation . The miR‐340 family was rated in the first position (Table ), and we are currently addressing this miR in a separate study.…”

Section: Resultsmentioning

confidence: 99%

miR‐29c improves skeletal muscle mass and function throughout myocyte proliferation and differentiation and by repressing atrophy‐related genes

et al. 2019

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AimTo identify microRNAs (miRs) involved in the regulation of skeletal muscle mass. For that purpose, we have initially utilized an in silico analysis, resulting in the identification of miR‐29c as a positive regulator of muscle mass.MethodsmiR‐29c was electrotransferred to the tibialis anterior to address its morphometric and functional properties and to determine the level of satellite cell proliferation and differentiation. qPCR was used to investigate the effect of miR‐29c overexpression on trophicity‐related genes. C2C12 cells were used to determine the impact of miR‐29c on myogenesis and a luciferase reporter assay was used to evaluate the ability of miR‐29c to bind to the MuRF1 3′UTR.ResultsThe overexpression of miR‐29c in the tibialis anterior increased muscle mass by 40%, with a corresponding increase in fibre cross‐sectional area and force and a 30% increase in length. In addition, satellite cell proliferation and differentiation were increased. In C2C12 cells, miR‐29c oligonucleotides caused increased levels of differentiation, as evidenced by an increase in eMHC immunostaining and the myotube fusion index. Accordingly, the mRNA levels of myogenic markers were also increased. Mechanistically, the overexpression of miR‐29c inhibited the expression of the muscle atrophic factors MuRF1, Atrogin‐1 and HDAC4. For the key atrogene MuRF1, we found that miR‐29c can bind to its 3′UTR to mediate repression.ConclusionsThe results herein suggest that miR‐29c can improve skeletal muscle size and function by stimulating satellite cell proliferation and repressing atrophy‐related genes. Taken together, our results indicate that miR‐29c might be useful as a future therapeutic device in diseases involving decreased skeletal muscle mass.

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Section: Resultsmentioning

confidence: 99%

miR‐29c improves skeletal muscle mass and function throughout myocyte proliferation and differentiation and by repressing atrophy‐related genes

et al. 2019

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“…In the proliferating cells, myogenic factor (Myf5) and MyoD were found to be co-expressed and bound to the same genes sites, whereas MyoD could more robustly recruit Pol II to bind the promoter of downstream genes 2 , including MyoG. As a myogenic regulator, MyoD possessed the ability of inducing cell cycle withdrawal to trigger differentiation 3–5 . Ablation of MyoD expression in C2C12 cells results in the inability to form myotubes, whereas remedial rescue can restore the ability to generate myotubes 6 .…”

Section: Introductionmentioning

confidence: 99%

Identification of MyoD-Responsive Transcripts Reveals a Novel Long Non-coding RNA (lncRNA-AK143003) that Negatively Regulates Myoblast Differentiation

Guo

Wang

Zhu

et al. 2017

Sci Rep

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Myogenic differentiation factor (MyoD) is a master transcription factor in muscle development and differentiation. Although several long non-coding RNAs (lncRNAs) linked to MyoD have been found to influence muscle development, the functions of many lncRNAs have not been explored. Here we utilized lncRNA and mRNA microarray analysis to identify potential lncRNAs regulated by MyoD in muscle cells. A total of 997 differentially expressed lncRNAs (335 up-regulated and 662 down-regulated) and 1,817 differentially expressed mRNAs (148 up-regulated and 1,669 down-regulated) were identified after MyoD knockdown in C2C12 cells. Functional predictions suggested that most lncRNAs are involved in the biological pathways related to muscle differentiation and cell cycle with co-expressed genes. To gain further insight into the MyoD-mediated lncRNA expression in muscle differentiation, tissue expression profiles and MyoD overexpression were performed, and we found one of the candidate lncRNAs-AK143003 was significantly regulated by MyoD. Further analyses showed its noncoding ability and cytoplasmic localisation. Silencing of AK143003 stimulated the accumulation of myogenic marker genes, whereas AK143003 overexpression led to their decreased synthesis. This study identified a multitude of MyoD-mediated lncRNAs for further investigation and identified a novel lncRNA, lnc-AK143003, which plays a role in controlling muscle differentiation.

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“…Although not selected for bioinformatics analysis in this study, the top-3 miRNAs displaying an increase in expression with age were members of the miR-29 family of miRNAs (mmu-miR-29a, rno-miR-29c# and mmu-miR-29c), supporting the important role played by this miRNA cluster in the myogenesis process. MiR-29a inhibition downregulates MyoD and upregulates cyclin-dependent kinase 6 ( Cdk6 ) expression in C 2 C 12 myoblasts, therefore delaying cell differentiation [53]. In contrast, miR-29 is upregulated in the muscle of aged when compared to young rodents.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA expression patterns in post-natal mouse skeletal muscle development

et al. 2017

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BackgroundMiRNAs are essential regulators of skeletal muscle development and homeostasis. To date, the role and regulation of miRNAs in myogenesis have been mostly studied in tissue culture and during embryogenesis. However, little information relating to miRNA regulation during early post-natal skeletal muscle growth in mammals is available. Using a high-throughput miRNA qPCR-based array, followed by stringent statistical and bioinformatics analysis, we describe the expression pattern and putative role of 768 miRNAs in the quadriceps muscle of mice aged 2 days, 2 weeks, 4 weeks and 12 weeks.ResultsForty-six percent of all measured miRNAs were expressed in mouse quadriceps muscle during the first 12 weeks of life. We report unprecedented changes in miRNA expression levels over time. The expression of a majority of miRNAs significantly decreased with post-natal muscle maturation in vivo. MiRNA clustering identified 2 subsets of miRNAs that are potentially involved in cell proliferation and differentiation, mainly via the regulation of non-muscle specific targets.ConclusionCollective miRNA expression in mouse quadriceps muscle is subjected to substantial levels of regulation during the first 12 weeks of age. This study identified a new suite of highly conserved miRNAs that are predicted to influence early muscle development. As such it provides novel knowledge pertaining to post-natal myogenesis and muscle regeneration in mammals.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3399-2) contains supplementary material, which is available to authorized users.

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<i>MyoD</i> is regulated by the miR-29a-<i>Tet1</i> pathway in C2C12 myoblast cells

Cited by 8 publications

References 37 publications

miR‐29c improves skeletal muscle mass and function throughout myocyte proliferation and differentiation and by repressing atrophy‐related genes

miR‐29c improves skeletal muscle mass and function throughout myocyte proliferation and differentiation and by repressing atrophy‐related genes

Identification of MyoD-Responsive Transcripts Reveals a Novel Long Non-coding RNA (lncRNA-AK143003) that Negatively Regulates Myoblast Differentiation

MicroRNA expression patterns in post-natal mouse skeletal muscle development

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