CCAAT/enhancer binding protein β is required for satellite cell self-renewal

Lala-Tabbert, Neena; AlSudais, Hamood; Marchildon, François; Fu, Dianzheng; Wiper‐Bergeron, Nadine

doi:10.1186/s13395-016-0112-8

Cited by 15 publications

(15 citation statements)

References 43 publications

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“…Therefore, these results indicate that Notch1 and Notch2 are crucial for maintaining the proliferative state of satellite cell‐derived myoblasts, although Notch3 may have the opposite function, acting as a repressor of satellite cell‐population expansion . A recent study reported that C/EBPβ, a transcription factor CCAAT/enhancer binding protein β, acts as a direct positive regulator for Notch2 expression but not for Notch1 and Notch3 , controlling satellite‐cell self‐renewal during muscle regeneration . Interestingly, Bi et al have reported stage specific roles of Notch1 during myogenesis .…”

Section: Discussionmentioning

confidence: 92%

Notch1 and Notch2 Coordinately Regulate Stem Cell Function in the Quiescent and Activated States of Muscle Satellite Cells

et al. 2017

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Satellite cells, the muscle tissue stem cells, express three Notch receptors (Notch1-3). The function of Notch1 and Notch2 in satellite cells has to date not been fully evaluated. We investigated the role of Notch1 and Notch2 in myogenic progression in adult skeletal muscle using tamoxifen-inducible satellite cell-specific conditional knockout mice for Notch1 (N1-scKO), Notch2 (N2-scKO), and Notch1/Notch2 (scDKO). In the quiescent state, the number of satellite cells was slightly reduced in N2-scKO, but not significantly in N1-scKO, and almost completely depleted in scDKO mice. N1-scKO and N2-scKO mice both exhibited a defect in muscle regeneration induced by cardiotoxin injection, while muscle regeneration was severely compromised with marked fibrosis in scDKO mice. In the activated state, ablation of either Notch1 or Notch2 alone in satellite cells prevented population expansion and self-renewal but induced premature myogenesis. Therefore, our results indicate that Notch1 and Notch2 coordinately maintain the stem-cell pool in the quiescent state by preventing activation and regulate stem-cell-fate decision in the activated state, governing adult muscle regeneration. Stem Cells 2018;36:278-285.

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Section: Discussionmentioning

confidence: 92%

Notch1 and Notch2 Coordinately Regulate Stem Cell Function in the Quiescent and Activated States of Muscle Satellite Cells

et al. 2017

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“…In vivo , loss of C/EBPβ in satellite cells results in larger myofibers and enhanced regenerative capacity after a single injury 22 . However, in this model, muscle regeneration was defective after a second injury due to impaired self-renewal and a reduction in the satellite cell pool supporting repair 23 . Although the role of C/EBPβ in satellite cell function has been elucidated, the specific mechanism by which C/EBPβ inhibits myogenic differentiation remains unknown.…”

Section: Introductionmentioning

confidence: 81%

CCAAT/Enhancer Binding Protein β inhibits myogenic differentiation via ID3

AlSudais

Lala-Tabbert

Wiper‐Bergeron

2018

Sci Rep

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Myogenesis is regulated by the coordinated expression of muscle regulatory factors, a family of transcription factors that includes MYOD, MYF5, myogenin and MRF4. Muscle regulatory factors are basic helix-loop-helix transcription factors that heterodimerize with E proteins to bind the regulatory regions of target genes. Their activity can be inhibited by members of the Inhibitor of DNA binding and differentiation (ID) family, which bind E-proteins with high affinity, thereby preventing muscle regulatory factor-dependent transcriptional responses. CCAAT/Enhancer Binding protein beta (C/EBPβ) is a transcription factor expressed in myogenic precursor cells that acts to inhibit myogenic differentiation, though the mechanism remains poorly understood. We identify Id3 as a novel C/EBPβ target gene that inhibits myogenic differentiation. Overexpression of C/EBPβ stimulates Id3 mRNA and protein expression, and is required for C/EBPβ-mediated inhibition of myogenic differentiation. Misexpression of C/EBPβ in myogenic precursors, such as in models of cancer cachexia, prevents the differentiation of myogenic precursors and we show that loss of Id3 rescues differentiation under these conditions, suggesting that the stimulation of Id3 expression by C/EBPβ is an important mechanism by which C/EBPβ inhibits myogenic differentiation.

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“…The expression of C/EBPβ was also positively modulated in SOL muscles of HFD rats. However, the increased C/EBPβ expression in leukocyte-derived RNA samples were previously associated with increased muscle strength in humans ( Harries et al, 2012 ) and enhanced satellite self-renewal leading to muscle regeneration in mice ( Lala-Tabbert et al, 2016 ). Conversely, C/EBPβ is also involved in the process through which pre-adipocytes are differentiated toward a mature adipocyte phenotype ( Tanaka et al, 1997 ).…”

Section: Discussionmentioning

confidence: 99%

Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

et al. 2018

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Obesity and ensuing disorders are increasingly prevalent in young populations. Prolonged exposure to high-fat diets (HFD) and excessive lipid accumulation were recently suggested to impair skeletal muscle functions in rodents. We aimed to determine the effects of a short-term HFD on skeletal muscle function in young rats. Young male Wistar rats (100–125 g) were fed HFD or a regular chow diet (RCD) for 14 days. Specific force, resistance to fatigue and recovery were tested in extensor digitorum longus (EDL; glycolytic) and soleus (SOL; oxidative) muscles using an ex vivo muscle contractility system. Muscle fiber typing and insulin signaling were analyzed while intramyocellular lipid droplets (LD) were characterized. Expression of key markers of lipid metabolism was also measured. Weight gain was similar for both groups. Specific force was decreased in SOL, but not in EDL of HFD rats. Muscle resistance to fatigue and force recovery were not altered in response to the diets. Similarly, muscle fiber type distribution and insulin signaling were not influenced by HFD. On the other hand, percent area and average size of intramyocellular LDs were significantly increased in the SOL of HFD rats. These effects were consistent with the increased expression of several mediators of lipid metabolism in the SOL muscle. A short-term HFD impairs specific force and alters lipid metabolism in SOL, but not EDL muscles of young rats. This indicates the importance of clarifying the early mechanisms through which lipid metabolism affects skeletal muscle functions in response to obesogenic diets in young populations.

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CCAAT/enhancer binding protein β is required for satellite cell self-renewal

Cited by 15 publications

References 43 publications

Notch1 and Notch2 Coordinately Regulate Stem Cell Function in the Quiescent and Activated States of Muscle Satellite Cells

Notch1 and Notch2 Coordinately Regulate Stem Cell Function in the Quiescent and Activated States of Muscle Satellite Cells

CCAAT/Enhancer Binding Protein β inhibits myogenic differentiation via ID3

Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

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