MicroRNA-1 facilitates skeletal myogenic differentiation without affecting osteoblastic and adipogenic differentiation

Nakajima, Norio; Takahashi, Toshifumi; Kitamura, Ryoji; Isodono, Koji; Asada, Satoshi; Ueyama, Tomomi; Matsubara, Hiroaki; Oh, Hidemasa

doi:10.1016/j.bbrc.2006.09.153

Cited by 70 publications

(42 citation statements)

References 24 publications

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“…Recent studies reveal that muscle-specific miRNA can also play important and varied roles in myogenesis (15,27,28,33,(55)(56)(57). These include: promotion of myoblast proliferation by miR-133-mediated suppression of serum response factor (27); initiation of cell cycle withdrawal by miR-206-mediated inhibition of the p180 sub- unit of DNA polymerase ␣ (15); and promotion of muscle differentiation by miR-1-mediated inhibition of the known transcriptional repressor of muscle-gene expression, HDAC4 (27).…”

Section: Discussionmentioning

confidence: 99%

“…Regardless of the mechanism by which post-transcriptional gene silencing occurs, the continuous identification of bioinformatically predicted and experimentally validated miRNA suggests that they play important and diverse biological roles in most eukaryotic species. Such roles include developmental timing (18), insulin secretion (19), oncogenesis (20 -24), and cellular differentiation including hematopoietic cell differentiation (25), adipogenesis (26), and myogenesis (15,(27)(28)(29).…”

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confidence: 99%

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MicroRNA-26a Targets the Histone Methyltransferase Enhancer of Zeste homolog 2 during Myogenesis

Wong

Tellam

2008

Journal of Biological Chemistry

291

235

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MicroRNA (miRNA) are important regulators of many biological processes, but the targets for most miRNA are still poorly defined. In this study, we profiled the expression of miRNA during myogenesis, from proliferating myoblasts through to terminally differentiated myotubes. Microarray results identified six significantly differentially expressed miRNA that were more than 2-fold different in myotubes. From this list, miRNA-26a (miR-26a), an up-regulated miRNA, was further examined. Overexpression of miR-26a in murine myogenic C2C12 cells induced creatine kinase activity, an enzyme that markedly increases during myogenesis. Further, myoD and myogenin mRNA expression levels were also up-regulated. These results suggest that increased expression of miR-26a promotes myogenesis. Through a bioinformatics approach, we identified the histone methyltransferase, Enhancer of Zeste homolog 2 (Ezh2), as a potential target of miR-26a. Overexpression of miR-26a suppressed the activity of a luciferase reporter construct fused with the 3-untranslated region of Ezh2. In addition, miR-26a overexpression decreased Ezh2 mRNA expression. These results reveal a model of regulation during myogenesis whereby the up-regulation of miR-26a acts to post-transcriptionally repress Ezh2, a known suppressor of skeletal muscle cell differentiation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

MicroRNA-26a Targets the Histone Methyltransferase Enhancer of Zeste homolog 2 during Myogenesis

Wong

Tellam

2008

Journal of Biological Chemistry

291

235

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“…Specifically, overexpression of either miR-1 or miR-206 decreased C2C12 cell proliferation and induced myogenesis. 1,8,9 miR-1 and miR-206 share extensive sequence identity and presumably regulate a similar spectrum of targets. In contrast, overexpression of miR-133 enhanced proliferation and inhibited myogenesis.…”

Section: Micrornas and Cellular Differentiationmentioning

confidence: 99%

MicroRNAs and Cell Cycle Regulation

Carleton¹,

Cleary²,

Linsley³

2007

Cell Cycle

320

205

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“…The fusion index was calculated according to the modified method of Nakajima et al (2006). C2C12 cells undergoing differentiation were fixed with 4 % paraformaldehyde for 30 min at 37°C and stained with DAPI solution (Wako Pure Chemical Industries).…”

Section: Fusion Indexmentioning

confidence: 99%

A novel in vitro model of sarcopenia using BubR1 hypomorphic C2C12 myoblasts

et al. 2015

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Sarcopenia is the age-related loss of skeletal muscle mass and function with adverse outcomes that include physical disability, poor quality of life, and death. The detailed molecular mechanisms remain unknown. An in vitro muscle atrophy model is needed to enable mechanistic studies. To create such a model, we employed BubR1 insufficiency which causes premature ageing in mice. Using C2C12 cells, a recognized in vitro model of the skeletal muscle cell, we obtained the BubR1 hypomorphic C2C12 (C2C12BKD) cells by using shRNA. The resulting C2C12BKD cells displayed several characteristics of the sarcopenic muscle cell. In C2C12BKD cells, formation of myotubes, assessed by analysis of fusion index, was markedly reduced as was the expression of myogenin and MyoD, two marker genes for myogenesis. Moreover, the cells showed increased expression of the muscle-specific ubiquitin ligases Atrogin-1 and MuRF-1, indicating increased protein degradation through the ubiquitin-proteasome dependent proteolytic pathway. These results suggest that C2C12BKD cells are potentially useful as a novel in vitro model of sarcopenia.

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MicroRNA-1 facilitates skeletal myogenic differentiation without affecting osteoblastic and adipogenic differentiation

Cited by 70 publications

References 24 publications

MicroRNA-26a Targets the Histone Methyltransferase Enhancer of Zeste homolog 2 during Myogenesis

MicroRNA-26a Targets the Histone Methyltransferase Enhancer of Zeste homolog 2 during Myogenesis

MicroRNAs and Cell Cycle Regulation

A novel in vitro model of sarcopenia using BubR1 hypomorphic C2C12 myoblasts

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