Molecular mechanisms implicated in myogenic differentiation of human alveolar mucosa derived cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE134207 | GEO | 2019/07/13
REPOSITORIES: GEO
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Project description:Skeletal muscle differentiation is a highly coordinated multistep process in which proliferating mononucleated myoblasts first withdraw from the cell cycle, then differentiate into postmitotic mononucleated myocytes, and subsequently fuse into multinucleated myotubes which finally bundle to form mature muscle fibers. All these processes are controlled by the sequential activation of myogenic regulatory factors, and especially MYOD1 is activated in the early phase to promote the transcription of muscle-specific genes coding for muscle proteins such as alpha-actin, myosin heavy chain and muscle creatine kinase. We used microarrays to detail the global gene expression changes associated with MYOD1 L122R mutation and identified MYOD1 L122R blocked myogenic differentiation and had a MYC-like transcriptional potential. C2C12 mouse myoblast cells were introduced wild type MYOD1, MYOD1 L122R, MYC, and GFP by retroviral infection. For retrovirus production, the pcx4 and pBabe vectors system were used. Retroviruses were obtained by using 293T cells as packaging cells, and were infected into C2C12 cell line and selected with 500 μg/ml Zeocin (Invitrogen, Carlsbad, CA, USA). After selection, RNAs were extracted and processed at MSKCC according to procedures recommended by Affymetrix (Santa Clara, CA, USA).
2014-05-01 | E-GEOD-56079 | biostudies-arrayexpress
Project description:Skeletal muscle differentiation is a highly coordinated multistep process in which proliferating mononucleated myoblasts ?rst withdraw from the cell cycle, then differentiate into postmitotic mononucleated myocytes, and subsequently fuse into multinucleated myotubes which ?nally bundle to form mature muscle ?bers. All these processes are controlled by the sequential activation of myogenic regulatory factors, and especially MYOD1 is activated in the early phase to promote the transcription of muscle-specific genes coding for muscle proteins such as alpha-actin, myosin heavy chain and muscle creatine kinase. We used microarrays to detail the global gene expression changes associated with MYOD1 L122R mutation and identified MYOD1 L122R blocked myogenic differentiation and had a MYC-like transcriptional potential. wild type MYOD1, MYOD1 L122R, MYC, and GFP were introduced into BJ human fibroblast cells by retroviral infection. For retrovirus production, the pcx4 and pBabe vectors system were used. Retroviruses were obtained by using 293T cells as packaging cells, and were infected into BJ cell lines and selected with 500 ?g/ml Zeocin (Invitrogen, Carlsbad, CA, USA). After selection, RNAs were extracted and processed at MSKCC according to procedures recommended by Affymetrix (Santa Clara, CA, USA).
2014-05-01 | E-GEOD-56078 | biostudies-arrayexpress
Project description:Abstract Hippo pathway downstream effectors Yap and Taz play key roles in cell proliferation and regeneration, regulating gene expression especially via interaction with Tead transcription factors. To investigate their role in skeletal muscle stem cells, we analysed Taz in vivo and ex vivo in comparison to Yap. Taz was expressed in activated satellite cells. siRNA knockdown or constitutive expression of wildtype or constitutively active TAZ mutants showed that TAZ promoted proliferation, a function that was shared with YAP. However, at later stages of myogenesis, TAZ also enhanced myogenic differentiation of myoblasts, whereas YAP inhibits such differentiation. Functionally, while muscle growth was mildly affected in Taz (gene symbol Wwtr1-/-) knockout mice, there were no overt effect on regeneration. However, conditional knockout of Yap in satellite cells of Pax7Cre-ERT2/+ : Yapflox/flox : Rosa26Lacz mice produced a marked regeneration deficit. To identify potential mechanisms, microarray analysis showed many common Taz/Yap targets, but Taz also regulates some genes independently of Yap, including myogenic genes such as Pax7, Myf5 and Myod1. Proteomic analysis of Yap/Taz revealed many common binding partners, but Taz also interacts with proteins distinct from Yap, that are mainly involved in myogenesis and aspects of cytoskeleton organization. Neither TAZ nor YAP bind members of the Wnt destruction complex but both extensively changed expression of Wnt and Wnt-cross talking genes with known roles in myogenesis. Finally, TAZ operates through Tead4 to enhance myogenic differentiation. In summary, Taz and Yap have overlapping functions in promoting myoblast proliferation but Taz then switches to promote myogenic differentiation.
2017-06-13 | PXD005751 | Pride
Project description:Skeletal muscle differentiation is a highly coordinated multistep process in which proliferating mononucleated myoblasts first withdraw from the cell cycle, then differentiate into postmitotic mononucleated myocytes, and subsequently fuse into multinucleated myotubes which finally bundle to form mature muscle fibers. All these processes are controlled by the sequential activation of myogenic regulatory factors, and especially MYOD1 is activated in the early phase to promote the transcription of muscle-specific genes coding for muscle proteins such as alpha-actin, myosin heavy chain and muscle creatine kinase. We used microarrays to detail the global gene expression changes associated with MYOD1 L122R mutation and identified MYOD1 L122R blocked myogenic differentiation and had a MYC-like transcriptional potential.
2014-05-01 | GSE56079 | GEO
Project description:Skeletal muscle differentiation is a highly coordinated multistep process in which proliferating mononucleated myoblasts first withdraw from the cell cycle, then differentiate into postmitotic mononucleated myocytes, and subsequently fuse into multinucleated myotubes which finally bundle to form mature muscle fibers. All these processes are controlled by the sequential activation of myogenic regulatory factors, and especially MYOD1 is activated in the early phase to promote the transcription of muscle-specific genes coding for muscle proteins such as alpha-actin, myosin heavy chain and muscle creatine kinase. We used microarrays to detail the global gene expression changes associated with MYOD1 L122R mutation and identified MYOD1 L122R blocked myogenic differentiation and had a MYC-like transcriptional potential.
2014-05-01 | GSE56078 | GEO
Project description:In the present study we show that the master myogenic regulatory factor, MYOD1, is a positive modulator of molecular clock amplitude and functions with the core clock factors for expression of clock-controlled genes in skeletal muscle. We demonstrate that MYOD1 directly regulates the expression and circadian amplitude of the positive core clock factor Bmal1. We identify a non-canonical E-box element in Bmal1 and demonstrate that is required for full MYOD1-responsiveness. Bimolecular fluorescence complementation assays demonstrate that MYOD1 colocalizes with both BMAL1 and CLOCK throughout myonuclei. We demonstrate that MYOD1 and BMAL1:CLOCK work in a synergistic fashion through a tandem Ebox to regulate the expression and amplitude of the muscle specific clock-controlled gene, Titin-cap (Tcap). In conclusion, these findings reveal mechanistic roles for the muscle specific transcription factor MYOD1 in the regulation of amplitude of the molecular clock as well as synergistic regulation of clock-controlled genes in skeletal muscle.
2018-11-02 | GSE122082 | GEO
Project description:Skeletal muscle function and regenerative capacity decline during aging, yet factors driving these changes are incompletely understood. Muscle regeneration requires temporally coordinated transcriptional programs to drive myogenic stem cells to activate, proliferate, fuse to form myofibers, and to mature myonuclei, restoring muscle function after injury. We assessed global changes in myogenic transcription programs distinguishing muscle regeneration in aged mice from young mice by comparing pseudotime trajectories from single-nucleus RNA sequencing of myogenic nuclei. Aging-specific differences in coordinating myogenic transcription programs necessary for restoring muscle function occur following muscle injury, likely contributing to compromised regeneration in aged mice. Differences in pseudotime alignment of myogenic nuclei when comparing aged to young mice via Dynamic Time-Warping revealed pseudotemporal differences becoming progressively more severe as regeneration proceeds. Disruptions in timing of myogenic gene expression programs may contribute to incomplete skeletal muscle regeneration and declines in muscle function as organisms age.
2023-06-12 | GSE180225 | GEO
Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.
2017-09-13 | GSE94560 | GEO
Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.
2017-09-13 | GSE94558 | GEO
Project description:Protein-leucine supplement ingestion following strenuous endurance exercise accentuates skeletal-muscle protein synthesis and adaptive molecular responses, but the underlying transcriptome is uncharacterized. In a randomized single-blind triple-crossover design, 12 trained men completed 100 min of high-intensity cycling then ingested either 70/15/180/30g protein/leucine/carbohydrate/fat (15LEU), 23/5/180/30g (5LEU) or 0/0/274/30g (CON) beverages during the first 90 min of a 240-min recovery period. Vastus lateralis muscle samples (30 and 240-min post-exercise) underwent transcriptome analysis by microarray followed by bioinformatic analysis. Gene expression was regulated by Protein-leucine in a dose-dependent manner impacting the inflammatory response, muscle growth and development. At 30 min, 15LEU and 5LEU vs. CON activated transcriptome networks with geneset functions involving cell-cycle arrest (Z-score 2.0-2.7; P<0.01), leukocyte maturation (1.7; P=0.007), cell viability (2.4; P=0.005), promyogenic networks encompassing myocyte differentiation and myogenin (MYOD1, MYOG), and a proteinaceous extracellular matrix, adhesion, and development programme correlated with plasma lysine, arginine, tyrosine, taurine, glutamic acid, and asparagine concentrations. High protein-leucine dose (15LEU-5LEU) activated an IL1b-centered proinflammatory network and leukocyte migration, differentiation, and survival functions (2.0-2.6; <0.001). By 240 min, the protein-leucine transcriptome was anti-inflammatory and promyogenic (IL-6, NF-kβ, SMAD, STAT3 network inhibition), with overrepresented functions including decreased leukocyte migration and connective tissue development (-1.8-2.4; P<0.01), increased apoptosis of myeloid and muscle cells (2.2-3.0; P<0.002) and cell metabolism (2.0-2.4; P<0.01). The analysis suggests protein-leucine ingestion modulates inflammatory-myogenic regenerative processes during skeletal muscle recovery from endurance exercise. Further cellular and translational research is warranted to validate amino acid-mediated myeloid and myocellular mechanisms within skeletal-muscle functional plasticity. Total RNA obtained from isolated skeletal muscles
2015-11-23 | E-GEOD-44818 | biostudies-arrayexpress