Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA272745 | ENA |
REPOSITORIES: ENA
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Project description:Deconstruction of DNA methylation patterns during myogenesis reveals Myf5 super-enhancer hypomethylation in the establishment of the muscle lineage
| PRJNA266799 | ENA
Project description:Recent studies have indicated important roles for long noncoding RNAs (lncRNAs) as potential essential regulators of myogenesis and adult skeletal muscle regeneration. However, in vivo, the role and mechanism of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells (MuSCs) and myogenesis are still largely unknown. Here, we identified a skeletal muscle specific-enriched lncRNA (myogenesis-associated lncRNA, short for lnc-mg). In vivo, skeletal muscle conditional knockout of lnc-mg resulted in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promoted muscle hypertrophy in mice. In vitro analyses of primary skeletal muscle cells isolated from mice showed that expression of lnc-mg was increased gradually during myogenic differentiation and overexpressed lnc-mg improved cell differentiation. Mechanistically, lnc-mg promoted myogenesis, by functioning as a competing endogenous RNA (ceRNA) for miR-125b to control protein abundance of Igf2. These findings identify lnc-mg as a novel and important noncoding regulator for muscle cell differentiation and skeletal muscle development. In order to identify functional lncRNAs correlating with myogenesis, microarrays were performed to detect the lncRNAs expression profile in undifferentiated MuSCs (GM, growth media/GM) ) and differentiated MuSCs (DM, differentiation media/DM).
2017-03-01 | GSE93276 | GEO
Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is commonly used in the treatment of hormone-responsive cancers. The effects of tamoxifen in anabolic tissues harboring estrogen-receptors, such as skeletal muscle, are poorly understood. As estrogen and estrogen receptors play an important role in skeletal muscle development and repair, we hypothesize that tamoxifen may have specific effects on myogenesis, the developmental process underlying muscle cells differentiation and repair. Myogenesis is characterized by fine-tuned changes in protein expression as embryonic myoblasts and adult satellite cells transition from pluripotent stem cells to multinucleated, contractile muscle fibers: we undertake a quantitative proteomic analysis of tamoxifen-induced changes in developing skeletal muscle cells which we expect may also shed light on the effect of tamoxifen on muscle repair.
We report a tandem mass-tag (TMT) approach to tamoxifen-treated myogenesis in C2C12 cells, a well-characterized model of in vitro murine skeletal muscle differentiation. A longitudinal analysis of >10,000 proteins identified in C2C12 myogenesis revealed a novel subset of 1,239 myogenically-regulated proteins. This set of regulatory proteins clustered into five distinct longitudinal expression trends which significantly overlap those obtained in similar analyses performed in human myocytes. A longitudinal analysis of myogenesis in the presence of tamoxifen, when contrasted with a similar analysis in untreated myogenesis finds that while the vast majority of myogenically-regulated proteins were unaffected by tamoxifen treatment, specific pathways and networks are affected. We document a specific functional enrichment for adiponectin-signaling, whereby a set of 198 proteins were differentially expressed relative to controls at one or more stages of myogenesis, the majority of which were involved in steroid biosynthesis, lipid storage and/or metal ion homeostasis. Interestingly, the only protein that was differentially expressed in the tamoxifen-treated cells at every stage of myogenesis was metallothionein-1 (MT1). Elevated levels of MT1 have been correlated with tamoxifen resistance and increased patient mortality and relapse in breast cancer, as well as with cachexia and muscle atrophy in rodent models. Increased MT1 expression levels may contribute to the musculoskeletal effects reported by patients undergoing tamoxifen treatment. Finally, we present a powerful, self-validating pipeline for analyzing the total proteomic response to in vitro treatment across every stage of muscle cells development which can be easily adapted to study the effects of other drugs on myogenesis.
2023-06-07 | MSV000092126 | MassIVE
Project description:Recent studies have indicated important roles for long noncoding RNAs (lncRNAs) as potential essential regulators of myogenesis and adult skeletal muscle regeneration. However, in vivo, the role and mechanism of lncRNAs in myogenic differentiation of adult skeletal muscle stem cells (MuSCs) and myogenesis are still largely unknown. Here, we identified a skeletal muscle specific-enriched lncRNA (myogenesis-associated lncRNA, short for lnc-mg). In vivo, skeletal muscle conditional knockout of lnc-mg resulted in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promoted muscle hypertrophy in mice. In vitro analyses of primary skeletal muscle cells isolated from mice showed that expression of lnc-mg was increased gradually during myogenic differentiation and overexpressed lnc-mg improved cell differentiation. Mechanistically, lnc-mg promoted myogenesis, by functioning as a competing endogenous RNA (ceRNA) for miR-125b to control protein abundance of Igf2. These findings identify lnc-mg as a novel and important noncoding regulator for muscle cell differentiation and skeletal muscle development. In order to test the hypothesis that lnc-mg may function as a ceRNA leading to the liberation of corresponding miRNA-targeted transcripts, microarrays were performed to detect miRNAs expression in lnc-mg overexpression and lnc-mg knockdown C2C12 cells.
2017-03-01 | GSE93277 | GEO
Project description:Skeletal muscle stem cells (MuSC), also called satellite cells, are indispensable for maintenance and regeneration of adult skeletal muscles. Yet, a comprehensive picture of the regulatory events controlling the fate of MuSC is missing. Here, we determine the proteome of MuSC to design a loss-of-function screen, and identify 120 genes important for MuSC function including the arginine methyltransferase Prmt5. MuSC-specific inactivation of Prmt5 in adult mice prevents expansion of MuSC, abolishes long-term MuSC maintenance and abrogates skeletal muscle regeneration. Interestingly, Prmt5 is dispensable for proliferation and differentiation of Pax7(+) myogenic progenitor cells during mouse embryonic development, indicating significant differences between embryonic and adult myogenesis. Mechanistic studies reveal that Prmt5 controls proliferation of adult MuSC by direct epigenetic silencing of the cell cycle inhibitor p21. We reason that Prmt5 generates a poised state that keeps MuSC in a standby mode, thus allowing rapid MuSC amplification under disease conditions.
2015-03-13 | GSE66822 | GEO
Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.
2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress
Project description:Muscle satellite cells (MuSCs), skeletal muscle-resident stem cells, are crucial for regeneration of myofibers. Mechanical cues are thought to be important for activation and proliferation of muscle satellite cells, but the molecular entity that senses biophysical forces in MuSCs remains to be elucidated. In this study, we identified PIEZO1, a mechanosensitive ion channel that is activated by membrane tension, as a critical determinant for myofiber regeneration. We investigated gene profiles of Piezo1-deficient MuSCs to understand the role of PIEZO1 during myogenesis. Our results suggest that PIEZO1 governs the cytoskeletal reorganization to regulate cellular events in MuSCs (i.e., activation, cell-division, and proliferation) during skeletal muscle regeneration.
2022-11-18 | GSE217417 | GEO
Project description:Fetal myogenesis and postnatal skeletal muscle hypertrophy in growing pigs are critical yet poorly understood processes. Global gene expression analyses will increase understanding of these processes by identifying key genes and pathways controlling skeletal muscle development. For this study, a pig 70-mer oligonucleotide microarray was used to identify differentially expressed genes in hind limb skeletal muscle of pigs at 60 days of gestation and 7 weeks of age. This oligonucleotide microarray experiment revealed 162 genes that were differentially expressed between 60 day fetal and 7 week postnatal samples. Relative real-time RT-PCR was used to confirm differential expression of three genes. This experiment identified genes exhibiting different developmental patterns of gene expression in pig skeletal muscle. Keywords: developmental study
2006-09-01 | GSE4958 | GEO
Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.
2012-04-30 | E-GEOD-36077 | biostudies-arrayexpress
Project description:Metabolic responses begin promptly upon the initiation of infection, and progress as a series of coordinated events. Mitochondria may play a key role in the development of insulin resistance. Reduced energy production and mitochondrial dysfunctional may further favor infection, and be an important step in the establishment of chronic and persistent infections. We have used mouse skeletal muscle transcriptome data which have led to the hypothesis that 2-AA causes harm to the host by triggering mitochondrial dysfunction in skeletal muscle. The gastrocnemius muscles were isolated from control and 4days 2-AA treated mouse for RNA extraction and hybridization on Affymetrix microarrays.
2013-01-28 | E-GEOD-43779 | biostudies-arrayexpress