Induction of CCAAT/Enhancer-Binding Protein β Expression With the Phosphodiesterase Inhibitor Isobutylmethylxanthine Improves Myoblast Engraftment Into Dystrophic Muscle

Lala-Tabbert, Neena; Fu, Dianzheng; Wiper‐Bergeron, Nadine

doi:10.5966/sctm.2015-0169

Cited by 13 publications

(16 citation statements)

References 52 publications

(92 reference statements)

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“…C/EBPβ has been shown have high expression in MuSCs and declines during early differentiation (Marchildon et al, 2012). Overexpression of C/EBPβ has been shown to inhibit myogenic differentiation, while loss of C/EBPβ leads to precocious differentiation (Lala-Tabbert et al, 2016). These data highlight the role of C/EBPs in preserving the stem/progenitor cell chromatin state.…”

Section: Resultsmentioning

confidence: 99%

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Glucose Metabolism Drives Histone Acetylation Landscape Transitions that Dictate Muscle Stem Cell Function

et al. 2019

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SUMMARYThe impact of glucose metabolism on muscle regeneration remains unresolved. We identify glucose metabolism as a crucial driver of histone acetylation and myogenic cell fate. We use single-cell mass cytometry (CyTOF) and flow cytometry to characterize the histone acetylation and metabolic states of quiescent, activated, and differentiating muscle stem cells (MuSCs). We find glucose is dispensable for mitochondrial respiration in proliferating MuSCs, so that glucose becomes available for maintaining high histone acetylation via acetyl-CoA. Conversely, quiescent and differentiating MuSCs increase glucose utilization for respiration and have consequently reduced acetylation. Pyruvate dehydrogenase (PDH) activity serves as a rheostat for histone acetylation and must be controlled for muscle regeneration. Increased PDH activity in proliferation increases histone acetylation and chromatin accessibility at genes that must be silenced for differentiation to proceed, and thus promotes self-renewal. These results highlight metabolism as a determinant of MuSC histone acetylation, fate, and function during muscle regeneration.

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Section: Resultsmentioning

confidence: 99%

“…This non-swelling gel chemistry results in equivalent laminin protein concentrations (estimated to be 7.5 ng cm–2 in ref. 32) on both soft and rigid hydrogels. We cut and adhered all hydrogels to cover the surface area (2.0 cm2) of 24-well culture plates.…”

Section: Methodsmentioning

confidence: 99%

Glucose Metabolism Drives Histone Acetylation Landscape Transitions that Dictate Muscle Stem Cell Function

et al. 2019

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“…A recent study examining human MuSC heterogeneity identified a population of CAV1+ MuSCs (CXCR4/CD29/CD56/CAV1) that were resistant to activation upon isolation and showed improved engraftment after transplantation, 48 a phenotype similar to C/EBPβ‐overexpressing primary myoblasts (Figure 3). 35 Thus, we next investigated the role of Cav1 in the C/EBPβ‐growth arrest phenotype.…”

Section: Resultsmentioning

confidence: 99%

CCAAT/enhancer-binding protein beta promotes muscle stem cell quiescence through regulation of quiescence-associated genes

et al. 2020

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Regeneration of skeletal muscle depends on resident muscle stem cells called satellite cells that in healthy, uninjured muscle remain quiescent (noncycling). After activation and expansion of satellite cells postinjury, satellite cell numbers return to uninjured levels and return to mitotic quiescence. Here, we show that the transcription factor CCAAT/enhancer-binding protein beta (C/EBPβ) is required to maintain quiescence of satellite cells in uninjured muscle. We show that C/EBPβ is expressed in quiescent satellite cells in vivo and upregulated in noncycling myoblasts in vitro. Loss of C/EBPβ in satellite cells promotes their premature exit from quiescence resulting in spontaneous activation and differentiation of the stem cell pool. Forced expression of C/EBPβ in myoblasts inhibits proliferation by upregulation of 28 quiescence-associated genes. Furthermore, we find that caveolin-1 is a direct transcriptional target of C/EBPβ and is required for cell cycle exit in muscle satellite cells expressing C/EBPβ. The induction of mitotic quiescence is considered necessary for the long-term maintenance of adult stem cell populations with dysregulation driving increased differentiation of progenitors and depletion of the stem cell pool. Our findings place C/EBPβ as an important transcriptional regulator of muscle satellite cell quiescence.

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“…C/ EBPβ is a member of a transcription factor family that takes part in the cell migration process [3,12,18]. Induction of C/EBPβ in muscle stem cells enhanced their migration and contributed to muscle repair in dystrophic muscle [12]. C/EBPβ is an important mediator in endothelial migration during pathological angiogenesis [18].…”

Section: Discussionmentioning

confidence: 99%

Cilostazol Promotes the Migration of Brain Microvascular Endothelial Cells

Lee¹,

Park²,

Shin³

2016

Journal of Life Science

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Cilostazol is known to be a selective inhibitor of phosphodiesterase III and is generally used to treat stroke. Our previous findings showed that cilostazol enhanced capillary density through angiogenesis after focal cerebral ischemia. Angiogenesis is an important physiological process for promoting revascularization to overcome tissue ischemia. It is a multistep process consisting of endothelial cell proliferation, migration, and tubular structure formation. Here, we examined the modulatory effect of cilostazol at each step of the angiogenic mechanism by using human brain microvascular endothelial cells (HBMECs). We found that cilostazol increased the migration of HBMECs in a dose-dependent manner. However, it did not enhance HBMEC proliferation and capillary-like tube formation. We used a cDNA microarray to analyze the mechanisms of cilostazol in cell migration. We picked five candidate genes that were potentially related to cell migration, and we confirmed the gene expression levels by real-time PCR. The genes phosphoserine aminotransferase 1 (PSAT1) and CCAAT/enhancer binding protein β (C/EBPβ) were up-regulated. The genes tissue factor pathway inhibitor 2 (TFPI2), retinoic acid receptor responder 1 (RARRES1), and RARRES3 were down-regulated. Our observations suggest that cilostazol can promote angiogenesis by promoting endothelial migration. Understanding the cilostazol-modulated regulatory mechanisms in brain endothelial cells may help stimulate blood vessel formation for the treatment of ischemic diseases.

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Induction of CCAAT/Enhancer-Binding Protein β Expression With the Phosphodiesterase Inhibitor Isobutylmethylxanthine Improves Myoblast Engraftment Into Dystrophic Muscle

Cited by 13 publications

References 52 publications

Glucose Metabolism Drives Histone Acetylation Landscape Transitions that Dictate Muscle Stem Cell Function

Glucose Metabolism Drives Histone Acetylation Landscape Transitions that Dictate Muscle Stem Cell Function

CCAAT/enhancer-binding protein beta promotes muscle stem cell quiescence through regulation of quiescence-associated genes

Cilostazol Promotes the Migration of Brain Microvascular Endothelial Cells

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