E-GEOD-56787
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA244584
TISSUE(S): Myoblast, Muscle, Myotube
DISEASE(S): Facioscapulohumeral Dystrophy,Normal
PROVIDER: E-GEOD-56787 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
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| E-GEOD-56787-analysis-methods.tsv | Tabular | |||
| E-GEOD-56787-analytics.tsv | Tabular | |||
| E-GEOD-56787-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-56787-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-56787-analytics.tsv.unrounded | Tabular |
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Project description:DUX4-induced gene expression is the major molecular signature in FSHD skeletal muscle
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Project description:Facioscapulohumeral dystrophy (FSHD) is caused by decreased epigenetic repression of the D4Z4 macrosatellite array and recent studies have shown that this results in the expression of low levels of the DUX4 mRNA in skeletal muscle. Several other mechanisms have been suggested for FSHD pathophysiology and it remains unknown whether DUX4 expression can account for most of the molecular changes seen in FSHD. Since DUX4 is a transcription factor, we used RNA-seq to measure gene expression in muscle cells transduced with DUX4, and in muscle cells and biopsies from control and FSHD individuals. We show that DUX4 target gene expression is the major molecular signature in FSHD muscle together with a gene expression signature consistent with an immune cell infiltration. In addition, one unaffected individual without a known FSHD-causing mutation showed expression of DUX4 target genes. This individual has a sibling with FSHD and also without a known FSHD-causing mutation, suggesting the presence of yet unidentified modifier locus for DUX4 expression and FSHD. These findings demonstrate that expression of DUX4 accounts for the majority of the gene expression changes in FSHD skeletal muscle together with an immune cell infiltration. RNA-seq for muscle cells and biopsies from control and FSHD individuals.
2014-07-03 | E-GEOD-56787 | biostudies-arrayexpress
Project description:Skeletal muscle atrophy and weakness are major contributors to morbidity, prolonged recovery, and long-term disability across a wide range of diseases. Atrophy is caused by breakdown of sarcomeric proteins resulting in loss of muscle mass and strength. Molecular mechanism underlying the onset of muscle atrophy and its progression have been analysed in patients, mice, and cell culture but the complementarity of these model systems remains to be explored. Here, we applied deep-coverage transcriptomic and proteomic profiling to characterize dynamic changes during dexamethasone-induced atrophy in the widely used murine skeletal muscle cell line C2C12. Comparison with published datasets confirmed that muscle differentiation is well recapitulated in C2C12 myotubes. Under dexamethasone-induced treatment, this model was particularly suited to capture early atrophy events, prior to disassembly and degradation of sarcomeric proteins. We also identified alterations in mitochondrial gene expression and differential alternative splicing events during early-stage myotube atrophy. This dataset complements existing in vivo data and provides novel insights into the regulatory processes during skeletal muscle wasting.
2025-10-14 | PXD064871 | Pride
Project description:Facioscapulohumeral dystrophy (FSHD) is caused by decreased epigenetic repression of the D4Z4 macrosatellite array and recent studies have shown that this results in the expression of low levels of the DUX4 mRNA in skeletal muscle. Several other mechanisms have been suggested for FSHD pathophysiology and it remains unknown whether DUX4 expression can account for most of the molecular changes seen in FSHD. Since DUX4 is a transcription factor, we used RNA-seq to measure gene expression in muscle cells transduced with DUX4, and in muscle cells and biopsies from control and FSHD individuals. We show that DUX4 target gene expression is the major molecular signature in FSHD muscle together with a gene expression signature consistent with an immune cell infiltration. In addition, one unaffected individual without a known FSHD-causing mutation showed expression of DUX4 target genes. This individual has a sibling with FSHD and also without a known FSHD-causing mutation, suggesting the presence of yet unidentified modifier locus for DUX4 expression and FSHD. These findings demonstrate that expression of DUX4 accounts for the majority of the gene expression changes in FSHD skeletal muscle together with an immune cell infiltration.
2014-07-03 | GSE56787 | GEO
Project description:Skeletal muscle atrophy is a serious and highly prevalent condition that remains poorly understood at the molecular level. Previous work found that skeletal muscle atrophy involves an increase in skeletal muscle Gadd45a expression, which is necessary and sufficient for skeletal muscle fiber atrophy. However, the direct mechanism by which Gadd45a promotes skeletal muscle atrophy was unknown. To address this question, we biochemically isolated skeletal muscle fiber proteins that associate with Gadd45a as it induces skeletal muscle atrophy in living mice. We found that Gadd45a interacts with multiple proteins in skeletal muscle fibers, including, most prominently, the MAP kinase kinase kinase MEKK4. Furthermore, by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase activity, which is sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy. Together, these results identify a direct biochemical mechanism by which Gadd45a induces skeletal muscle atrophy and provide new insight into way that skeletal muscle atrophy occurs at the molecular level.
2016-05-17 | MSV000079730 | MassIVE
Project description:Regulated in DNA Damage and Development 1 (REDD1) is a stress induced protein whose expression is highly induced in skeletal muscle following a single bout of aerobic exercise. However, the role of this induction is unknown We used microarrays to detail the change in gene signature within skeletal muscle following a single bout of aerobic exercise in wild type and REDD1 null mice
2017-10-05 | GSE97415 | GEO
Project description:The nucleosome signature reflects the cellular epigenetic memory and contributes to the cellular phenotype and function. Obesity and type 2 diabetes pathogenesis is largely dependent on environmentally-induced epigenetic modifications and is marked by skeletal muscle insulin resistance; however, no in vivo skeletal muscle nucleosome maps exist to date. Herein, whole genome nucleosome maps via MNase-seq in skeletal muscle of mice on a low fat, high fat or high fat diet with the chromatin modifier sodium butyrate show that complex interactions among mitochondrial function, the tissue microenvironment, cellular phenotype and nucleosome landscape determine whole body phenotype and insulin resistance. Skeletal muscle samples (n=5 per group) were pooled after homogenization under liquid nitrogen with a motar and pestle to give one sample per group for MNase-seq
2012-05-11 | E-GEOD-37913 | biostudies-arrayexpress
Project description:Changes and plasticity in both gene expression and protein signaling in skeletal muscle is considered to be a major cause of metabolic syndrome, while it has been shown that mild exercise training at lactate threshold (LT) intensity is a safe and effective for prevention of metabolic syndrome. To elucidate the molecular mechanisms related to the beneficial effects of LT training for 60 min/day for 5 days/wk for 12 wk, we performed serial analysis of gene expression (SAGE) to examine global mRNA expression in human skeletal muscle. Approximately 57000 SAGE tags were analyzed for before training, as well as 5 days, 6 and 12 wk after the training. The LT training has coordinately induced many genes involved in mitochondrial energy metabolism, fat oxidation, glycolysis and creatine metabolism. Another molecular feature associated with this mild exercise regimen has been an induction of many genes encoding for potent antioxidant enzymes and molecular chaperons. Furthermore, the training modulated the expression levels of 233 novel transcripts. Thus, the current study reveals that LT exercise has favorably altered gene expression in human skeletal muscle to the prevention of metabolic syndrome. Keywords: transcriptome, serial analysis of gene expression, metabolic syndrome, exercise training, lactate threshold
2006-09-09 | GSE5792 | GEO
Project description:Skeletal muscle atrophy and weakness are major contributors to morbidity, prolonged recovery, and long-term disability across a wide range of diseases. Atrophy is caused by breakdown of sarcomeric proteins resulting in loss of muscle mass and strength. Molecular mechanism underlying the onset of muscle atrophy and its progression have been analysed in patients, mice, and cell culture but the complementarity of these model systems remains to be explored. Here, we applied deep-coverage transcriptomic and proteomic profiling to characterize dynamic changes during dexamethasone-induced atrophy in the widely used murine skeletal muscle cell line C2C12. Comparison with published datasets confirmed that muscle differentiation is well recapitulated in C2C12 myotubes. Under dexamethasone-induced treatment, this model was particularly suited to capture early atrophy events, prior to disassembly and degradation of sarcomeric proteins. We also identified alterations in mitochondrial gene expression and differential alternative splicing events during early-stage myotube atrophy. This dataset complements existing in vivo data and provides novel insights into the regulatory processes during skeletal muscle wasting.
2025-09-29 | GSE300503 | GEO
Project description:Background Loss of skeletal muscle mass in advanced cancer is recognized as an independent predictor of mortality. Mechanisms involved in this wasting process and parameters for early diagnosis are still lacking. As skeletal muscle is considered as a secretory organ, the aim of this present experimental work was to characterize the changes in muscle proteome and secretome associated with cancer-induced cachexia to better understand cellular mechanisms involved in this wasting process and to identify secreted proteins which might reflect the ongoing muscle atrophy process. Methods We investigated first the changes in the muscle proteome associated with cancer-induced cachexia by using differential label-free proteomic analysis on muscle of the C26 mouse model. The differentially abundant proteins were submitted to sequential bioinformatic secretomic analysis in order to identify potentially secreted proteins. Selected reaction monitoring and Western blotting were used to verify the presence of candidate proteins at the circulating level. Their muscle source was demonstrated by assessing their gene expression in skeletal muscle and in cultured myotubes. Finally, we also investigated their regulation in muscle cells. Alterations in several molecular pathways potentially involved in muscle atrophy were highlighted using Gene ontology enrichment analyses. Results Our results revealed a dramatic increased production (2-to 25-fold) by the muscle of several acute phase reactants (APR: Haptoglobin, Serpina3n, Complement C3, Serum amyloid A1) which are also released in the circulation during C26 cancer cachexia. Their production was confirmed in other preclinical models of cancer cachexia as well as in cancer patients. The muscular origin of these APR was demonstrated by their increased expression in skeletal muscle and myotubes. Glucocorticoids and pro-inflammatory cytokines contribute directly to their increased expression in muscle cells in vitro, while the role of IL-6 in the muscular induction of these APR was demonstrated in vivo. Conclusions Cancer is associated with marked changes in muscle secretome during muscle wasting. Our study demonstrates a marked increased production of APR by skeletal muscle in pre-clinical models of cancer cachexia and in cancer patients. Further studies are required to unravel the potential role of these proteins in muscle atrophy and their interest as biomarkers of cancer cachexia.
2020-10-28 | PXD016474 | Pride