Epigenetic regulation of satellite cell activation during muscle regeneration

Dilworth, F. Jeffrey; Blais, Alexandre

doi:10.1186/scrt59

Cited by 57 publications

(52 citation statements)

References 71 publications

(99 reference statements)

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“…Developmental and adult skeletal myogenesis are activated by the basic helix-loop-helix (bHLH) family of myogenic regulatory factors (MRFs), MyoD, Myf5, MRF4, and myogenin, which share the ability to promote transcription from E-box sequences (CAN-NTG) found in the regulatory region of many muscle-specific genes [1][2][3]. MRF competence to promote transcription of muscle genes relies on the interaction with the SWI/SNF chromatinremodeling complex [4,5].…”

Section: Introductionmentioning

confidence: 99%

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

et al. 2015

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Although the two catalytic subunits of the SWI/SNF chromatinremodeling complex-Brahma (Brm) and Brg1-are almost invariably co-expressed, their mutually exclusive incorporation into distinct SWI/SNF complexes predicts that Brg1-and Brm-based SWI/SNF complexes execute specific functions. Here, we show that Brg1 and Brm have distinct functions at discrete stages of muscle differentiation. While Brg1 is required for the activation of muscle gene transcription at early stages of differentiation, Brm is required for Ccnd1 repression and cell cycle arrest prior to the activation of muscle genes. Ccnd1 knockdown rescues the ability to exit the cell cycle in Brm-deficient myoblasts, but does not recover terminal differentiation, revealing a previously unrecognized role of Brm in the activation of late muscle gene expression independent from the control of cell cycle. Consistently, Brm null mice displayed impaired muscle regeneration after injury, with aberrant proliferation of satellite cells and delayed formation of new myofibers. These data reveal stage-specific roles of Brm during skeletal myogenesis, via formation of repressive and activatory SWI/SNF complexes.

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Section: Introductionmentioning

confidence: 99%

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

et al. 2015

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“…After re-neuralization, the residual SCs begin to proliferate and differentiate; under the innervation of the regenerated nerve, they form new muscle cells, or bind with the original muscle cells (the latter is the main mode of muscle regeneration after nerve regeneration, that is, hypertrophic muscle regeneration (Malatesta et al, 2011); and this can be used to explain the morphologic change of muscle regeneration in which cells in the muscle fascicle are different in size as newly-generated muscle fibers can only come from the differentiated SCs rather than the differentiation of the residual muscle fibers (Yamada et al, 1989;Dilworth & Blais, 2011;van der Meer et al, 2011). In the present study, the 2-month and 3 month groups showed better neuromuscular function recovery, and they also showed stronger cell differentiation abilities compared to other groups.…”

Section: Discussionmentioning

confidence: 99%

Correlation between Innervation of Skeletal Muscles and Myoblast Stem Cells

Sun

Zhu

et al. 2012

Int. J. Morphol.

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SUMMARY:In order to explore the change rule of myoblast stem cells (satellite cells, SCs) in the denervated and re-innervated muscle and to investigate the cellular mechanism of the morphological and functional changes of the muscle, denervated muscle atrophy and nerve regeneration models were established in one-month-old rats. Postoperative indexes such as muscle wet weight, cell section areas, content of collagen fibers and DNA, electrophysiology, numbers of SCs in the triceps muscle of calf were dynamically tested. After denervation, the muscle wet weight and cell area reduced rapidly, and the collagen fiber content increased slowly. The number of SCs increased at first, and then declined suddenly two months later. From 4 to 5 weeks after re-neuralization, muscle action potentials could be evoked, but the best innervation effect was found in the groups, which received re-neuralization at 2 months and 3 months after denervation. Denervation causes a progressive progress of muscle atrophy. SCs proliferate within 3 months after denervation, and then atrophy becomes irreversible from 4 months. At 4 or 5 weeks after re-neuralization, muscle action potentials can be evoked. Re-neuralization at 2 months and 3 months after denervation can achieve a good effect on the functional recovery of the atrophic muscle.

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“…Consistent with the notion that H3K4me3 alone does not predict the transcriptional state of a gene but rather marks the gene for transcriptional activation [61] , neither the number nor the identity of genes marked by H3K4me3 is significantly different between activated and quiescent SCs. Indeed, SC activation is accompanied by the retention of H3K4me3 and the acquisition of H3K27me3 via PcG members [62] , often in association with the transcriptional repressors YY1 and HDAC1. Interestingly, low levels of H3K27me3 are associated with the pluripotency of embryonic stem cells [56,63] .…”

Section: Noncoding Rnasmentioning

confidence: 99%

“…As a general rule, genes no longer required for lineage progression are targeted for stable repression [59,62] . Accordingly, during differentiation, SC chromatin converts to a more repressed state by accumulating H3K27me3 across the genome at both transcription start sites and intergenic regions.…”

Section: Epigenetic Control Of Sc Differentiationmentioning

confidence: 99%

New insights into the epigenetic control of satellite cells

Moresi

Marroncelli

Adamo

2015

WJSC

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Epigenetics finely tunes gene expression at a functional level without modifying the DNA sequence, thereby contributing to the complexity of genomic regulation. Satellite cells (SCs) are adult muscle stem cells that are important for skeletal post-natal muscle growth, homeostasis and repair. The understanding of the epigenome of SCs at different stages and of the multiple layers of the post-transcriptional regulation of gene expression is constantly expanding. Dynamic interactions between different epigenetic mechanisms regulate the appropriate timing of muscle-specific gene expression and influence the lineage fate of SCs. In this review, we report and discuss the recent literature about the epigenetic control of SCs during the myogenic process from activation to proliferation and from their commitment to a muscle cell fate to their differentiation and fusion to myotubes. We describe how the coordinated activities of the histone methyltransferase families Polycomb group (PcG), which represses the expression of developmentally regulated genes, and Trithorax group, which antagonizes the repressive activity of the PcG, regulate myogenesis by restricting gene expression in a time-dependent manner during each step of the process. We discuss how histone acetylation and deacetylation occurs in specific loci throughout SC differentiation to enable the time-dependent transcription of specific genes. Moreover, we describe the multiple roles of microRNA, an additional epigenetic mechanism, in regulating gene expression in SCs, by repressing or enhancing gene transcription or translation during each step of myogenesis. The importance of these epigenetic pathways in modulating SC activation and differentiation renders them as promising targets for disease interventions. Understanding the most recent findings regarding the epigenetic mechanisms that regulate SC behavior is useful from the perspective of pharmacological manipulation for improving muscle regeneration and for promoting muscle homeostasis under pathological conditions.

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Epigenetic regulation of satellite cell activation during muscle regeneration

Cited by 57 publications

References 71 publications

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis

Correlation between Innervation of Skeletal Muscles and Myoblast Stem Cells

New insights into the epigenetic control of satellite cells

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