Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enhanced energetic state and protection from oxidative stress in human myoblasts overexpressing BMI1

ABSTRACT: The Polycomb group gene BMI1 is essential for efficient muscle regeneration in a mouse model of Duchenne Muscular Dystrophy and its enhanced expression in adult skeletal muscle satellite cells ameliorates the muscle strength in this model. In this experiment, we investigated the impact of mild BMI1 overexpression in human cells. We showed translation between observed mouse and human phenotypes. In human myoblasts, BMI1 overexpression increases mitochondrial activity leading to an enhanced energetic state with increased ATP production and concomitant protection against DNA damage both in vitro and upon xenografting in a severe dystrophic mouse model. These preclinical data in mouse models and in human cells provide a strong rationale for the development of pharmacological approaches to target BMI1-mediated mitochondrial regulation and protection from DNA damage to sustain the regenerative potential of the skeletal muscle in conditions of chronic muscle wasting. This ArrayExpress record is for the RNA-seq data from three independently prepared normal and DMD myoblasts cell cultures infected with GFP and BMI1Over lentiviral particles and induced to differentiate for 2 days.

Please note that each biological sample has one library, and each library is sequenced with two NextSeq runs, each run on identical 4 lane configurations. Hence for each biological sample, there are 16 raw fastq files. The run and lane information has been captured in the “run batch” and “lane batch” attributes respectively in the samples table, and should be used for bath corrections during analysis.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Barnes

PROVIDER: E-MTAB-5846 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq data from healthy and DMD human cells, along skeletal muscle differentiation from induced pluripotent stem cells

Project description:3 healthy cells - 3 DMD cells - 7 time points (tissue-derived myoblasts, tissue-derived myotubes, hiPSCs, Day 3 of differentiation, Day 10 of differentiation, Day 17 of differentiation, Day 25 of differentiation) - 1 replicate per cell line for the tissue-derived samples and 3 biological replicates per cell line for the hiPSC-derived samples.

2020-10-05 | E-MTAB-8321 | biostudies-arrayexpress

miRNA-seq data from healthy and DMD human cells, along skeletal muscle differentiation from induced pluripotent stem cells

Project description:3 or 4 healthy cells - 3 DMD cells - 7 time points (tissue-derived myoblasts, tissue-derived myotubes, hiPSCs, Day 3 of differentiation, Day 10 of differentiation, Day 17 of differentiation, Day 25 of differentiation).

2020-10-05 | E-MTAB-8293 | biostudies-arrayexpress

ChIP-seq of GATA4 in mouse skeletal muscle myoblasts

Project description:GATA4 occupancy on the mouse genome of satellite cell-derived primary myoblasts. Proliferating myoblasts cultured in growth medium were immunoprecipitated with anti-GATA4 antibody or control IgG. Precipitated genomic DNAs were subjected to next generation sequencing. Paired-end 150 bp sequence reads of GATA4-ChIP and IgG-ChIP using mouse skeletal muscle myoblasts.

2015-04-10 | E-GEOD-67703 | biostudies-arrayexpress

A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation (RNA-seq)

Project description:The transcriptional activator MyoD serves as a master controller of myogenesis. Often in partnership with Mef2, MyoD binds to the promoters of hundreds of muscle genes in proliferating myoblasts, yet activates these targets only upon receiving cues that launch differentiation. What regulates this off/on switch of MyoD function has been incompletely understood, although known to reflect the action of chromatin modifiers. Here, we identify KAP1/TRIM28 as a key regulator of MyoD function. In myoblasts, KAP1 is present with MyoD and Mef2 at many muscle genes, where it acts as a scaffold to recruit not only co-activators such as p300 and LSD1, but also co-repressors such as G9a and HDAC1, with promoter silencing as net outcome. Upon differentiation, MSK1-mediated phosphorylation of KAP1 releases the co-repressors from the scaffold, unleashing transcriptional activation by MyoD/Mef2 and their positive cofactors. Thus, our results reveal KAP1 as a previously unappreciated interpreter of cell signaling, which modulates the ability of MyoD to drive myogenesis. Transcriptome profiling of control and Kap1KD in C2C12 during proliferation or at 48hours differentiation stage

2015-02-02 | E-GEOD-62659 | biostudies-arrayexpress

DUX4 activates germline genes, retroelements and immune-mediators: Implications for facioscapulohumeral dystrophy

Project description:Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited muscular dystrophies. The causative gene remains controversial and the mechanism of pathophysiology unknown. Here we identify genes associated with germline and early stem cell development as targets of the DUX4 transcription factor, a leading candidate gene for FSHD. The genes regulated by DUX4 are reliably detected in FSHD muscle but not in controls, providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD. Additionally, we show that DUX4 binds and activates LTR elements from a class of MaLR endogenous primate retrotransposons and suppresses the innate immune response to viral infection, at least in part through the activation of DEFB103, a human defensin that can inhibit muscle differentiation. These findings suggest specific mechanisms of FSHD pathology and identify candidate biomarkers for disease diagnosis and progression. [Overexpression experiment] Quadruplicate total RNA samples were collected from control human primary myoblasts transduced with lentivirus carrying DUX4-fl, DUX4-s or GFP (MOI = 15) for 24 h and from untransduced myoblasts. [Defensin experiment] Quadruplicate samples were also collected from myoblasts and myotubes grown in media containing human beta-defensin 3 peptide or in control media.

2012-01-03 | E-GEOD-33799 | biostudies-arrayexpress

miRNA mimic transfected SC and MIPC transcriptome analysis

Project description:In the present study, we analyzed two populations of myogenic cells isolated from mouse skeletal muscle, that is, myoblasts derived from satellite cells (SCs) and muscle interstitial progenitor cells (MIPCs). We found that SDF-1 treatment of myoblasts led to down-regulation of miR10a, miR151, miR425, and miR5100. Therefore, to follow the impact of these miRNAs on myogenic cells, SC-derived myoblasts and MIPCs were transfected with selected miRNA mimics in the concentration of 50 mol/L and changes in their transcriptome were analyzed.

2022-12-05 | E-MTAB-12500 | biostudies-arrayexpress

Genome-wide remodeling of the epigenetic landscape during myogenic differentiation

Project description:We have examined changes in the chromatin landscape during muscle differentiation by mapping the genome-wide location of ten key histone marks and transcription factors in mouse myoblasts and terminally differentiated myotubes, providing an exceptionally rich dataset that has enabled discovery of key epigenetic changes underlying myogenesis. Using this compendium, we focused on a well-known repressive mark, histone H3 lysine 27 trimethylation, and identified novel regulatory elements flanking the myogenin gene that function as a key differentiation-dependent switch during myogenesis. Next, we examined the role of Polycomb-mediated H3K27 methylation in gene repression by systematically ablating components of both PRC1 and PRC2 complexes. Surprisingly, we found mechanistic differences between transient and permanent repression of muscle differentiation and lineage commitment genes and observed that the loss of PRC1 and PRC2 components produced opposing differentiation defects. These phenotypes illustrate striking differences as compared to embryonic stem cell differentiation and suggest that PRC1 and PRC2 do not operate sequentially in muscle cells. Our studies of PRC1 occupancy also suggested a "fail-safe" mechanism, whereby PRC1/Bmi1 concentrates at genes specifying nonmuscle lineages, helping to retain H3K27me3 in the face of declining Ezh2-mediated methyltransferase activity in differentiated cells. Mapping of PoII, H3K4me1, H3K4me2, H3K4me3, H3K27me3, H3K36me3, H3K9Ac, H3K18Ac and H4K12Ac in growing myoblasts (MB) and fully differentiated myotubes (MT).

2011-05-08 | E-GEOD-25308 | biostudies-arrayexpress

Characteristics of the transcriptome of a nurse cell harboring muscle larva of Trichinella spiralis

Project description:Muscle larva of a parasitic nematode Trichinella spp. lives a portion of muscle fiber transformed to a nurse cell (NC). The NC is formed from miss-differentiated muscle satellite cells which have fused with a parasite-invaded degenerating myofiber. Though originating from muscle cells, the NC is of non-muscular type.The NC is multinuclear and hypertrophic. Molecular mechanism of the NC development remains largely unknown. The microarray project was aimed at characterization of the NC transcriptome. The NCs were isolated by enzymatic digestion from infected mouse striated muscles. Murine C2C12 myogenic cell line (ATCC) was cultured in vitro. Differentiation of myoblasts into myotubes was carried out for 6 days in a high-glucose DMEM supplemented with 2% heat-inactivated horse serum, on the plates covered with laminin and collagen IV.The NC transcriptome was referred to the transcriptomes of C2C12 myoblasts and C2C12 myotubes in two sets of camparative expression microarray hybridization experiments, NC vs myoblasts and NC vs myotubes, respectively.

2022-07-26 | E-MTAB-12042 | biostudies-arrayexpress

TGFbeta effect on human skeletal muscle primary cultured cells

Project description:In this experiment we have analyzed the effect of TGFbeta-1 incubation (3h of incubation time) on the gene expression profiles of human primary cultured skeletal muscle cells, both in growing myoblasts or in differentiated muscle fibres (after 10-days of differentiation), obtained from skeletal muscle biopsies from a 2-months old healthy donor and a 5-years old DMD (Duchenne Muscular Dystrophy) patient. All human skeletal muscle biopsies were obtained by surgery from calf muscles with informed consent and approval of the Human Use Committee of Vall d'Hebron University Hospital (Barcelona, Spain). Human myoblasts were cultured on 6 cm plates until reached 70-80% of confluence and then, were incubated for 3h in the presence or in absence of TGF-?1 (2.5 ng/ml). Skeletal muscle fibres were obtained by growing human myoblasts on 6 cm plates until reached 70-80% of confluence and then, cells were induced to differentiate by deprivation of growth factors in the culture medium. After 10 days of differentiation, skeletal muscle fibers were incubated for 3h in the presence or in absence of TGFbeta-1 (2.5 ng/ml). In all cases, immediately after TGFbeta-1 treatment the RNA was extracted and used for Affymetrix microarrays analysis using the U133 2.0 microarray genechips.

2016-08-07 | E-MEXP-2937 | biostudies-arrayexpress

Transcriptome-wide Regulation of Splicing and mRNA Localization by Muscleblind Proteins

Project description:The Muscleblind-like (Mbnl) family of RNA-binding proteins plays important roles in muscle and eye development and in Myotonic Dystrophy (DM), where expanded CUG or CCUG repeats functionally deplete Mbnl proteins. We identified transcriptome-wide functional and biophysical targets of Mbnl proteins in brain, heart, muscle, and myoblasts using RNA sequencing and crosslinking/immunoprecipitation-sequencing approaches. This analysis identified several hundred splicing events whose regulation depended on Mbnl function, in a pattern indicative of functional interchangeability between Mbnl1 and Mbnl2. A nucleotide resolution RNA map associated repression or activation of exon splicing with Mbnl binding near either 3' splice site or near the downstream 5' splice site, respectively. Transcriptomic analysis of sub-cellular compartments uncovered a global role for Mbnls in regulating localization of mRNAs encoding membrane, synaptic and other proteins in both mouse and Drosophila cells, and Mbnls also contribute to protein secretion. These findings hold several new implications for DM pathogenesis. To assess global functions of Muscleblind proteins, RNA-Seq was performed using WT and Mbnl1 KO brain, heart, and muscle (5 mice each). Additionally, C2C12 mouse myoblasts were depleted of Mbnl1, Mbnl2, or both. Subcellular fractionation experiments were performed to analyze mRNA localization following depletion of Mbnl1 and Mbnl2 in C2C12 mouse myoblasts, and following depletion of Mbnl in Drosophila S-2R+ cells. CLIP-Seq was also performed against Mbnl1 in mouse brain, heart, muscle, and C2C12 myoblasts. Finally, ribosome footprinting was performed with C2C12 mouse myoblasts that were depleted of Mbnl1, Mbnl2, or both.

2012-08-17 | E-GEOD-39911 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data