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Loss of full-length dystrophin expression causes major cell-autonomous abnormalities in proliferating myoblasts

ABSTRACT: Loss of full-length dystrophin expression causes major cell-autonomous abnormalities in proliferating myoblasts

PROVIDER: PRJEB44152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5671410_1.fastq.gz	Fastqsanger.gz
	ERR5671410_2.fastq.gz	Fastqsanger.gz
	ERR5671402_1.fastq.gz	Fastqsanger.gz
	ERR5671402_2.fastq.gz	Fastqsanger.gz
	ERR5671403_1.fastq.gz	Fastqsanger.gz

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Loss of full-length dystrophin expression causes major cell-autonomous abnormalities in proliferating myoblasts

Project description:Duchenne muscular dystrophy (DMD) is a severely debilitating and incurable neuromuscular disease. Its conspicuous feature is the absence of dystrophin in myofibers and therefore most therapeutic approaches focus on some form of its re-expression there. However, increasing body of evidence points at an early developmental onset of DMD and severe abnormalities were uncovered in dystrophic muscle stem cells. In this study, we explore gene expression changes in primary myoblasts from mice lacking expression of the full length dystrophin transcript. Total RNA extracted from primary myoblasts isolated from gastrocnemii of 8 week old male Dmd-mdx (MDX - lacking the full length dystrophin transcript), Dmd-mdx-βgeo (BGEO - lacking all dystrophin expression) and control mice (WT) were subjected to RNA sequencing following ribodepletion, and analysed for the differential expression of genes between groups and the enrichment of gene ontology categories or pathways.

2022-09-14 | E-MTAB-10322 | biostudies-arrayexpress

Loss of full-length dystrophin expression results in major cell-autonomous abnormalities in proliferating myoblasts.

Project description:Duchenne muscular dystrophy (DMD) affects myofibers and muscle stem cells, causing progressive muscle degeneration and repair defects. It was unknown whether dystrophic myoblasts-the effector cells of muscle growth and regeneration-are affected. Using transcriptomic, genome-scale metabolic modelling and functional analyses, we demonstrate, for the first time, convergent abnormalities in primary mouse and human dystrophic myoblasts. In Dmdmdx myoblasts lacking full-length dystrophin, the expression of 170 genes was significantly altered. Myod1 and key genes controlled by MyoD (Myog, Mymk, Mymx, epigenetic regulators, ECM interactors, calcium signalling and fibrosis genes) were significantly downregulated. Gene ontology analysis indicated enrichment in genes involved in muscle development and function. Functionally, we found increased myoblast proliferation, reduced chemotaxis and accelerated differentiation, which are all essential for myoregeneration. The defects were caused by the loss of expression of full-length dystrophin, as similar and not exacerbated alterations were observed in dystrophin-null Dmdmdx-βgeo myoblasts. Corresponding abnormalities were identified in human DMD primary myoblasts and a dystrophic mouse muscle cell line, confirming the cross-species and cell-autonomous nature of these defects. The genome-scale metabolic analysis in human DMD myoblasts showed alterations in the rate of glycolysis/gluconeogenesis, leukotriene metabolism, and mitochondrial beta-oxidation of various fatty acids. These results reveal the disease continuum: DMD defects in satellite cells, the myoblast dysfunction affecting muscle regeneration, which is insufficient to counteract muscle loss due to myofiber instability. Contrary to the established belief, our data demonstrate that DMD abnormalities occur in myoblasts, making these cells a novel therapeutic target for the treatment of this lethal disease.

| S-EPMC9514850 | biostudies-literature

RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

Project description:RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

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ChIP-seq Profiling of RXRα in Proliferating C2C12 Myoblasts

Project description:In this dataset, we present ChIP-seq profiling of RXRα in proliferating C2C12 myoblasts, which serves as an extension of Series GSE94558. The overall data provides genome-wide occupancy of RXRα in normal myoblast proliferation.

2024-10-31 | GSE279060 | GEO

ChIP-seq Profiling of RXRα in Proliferating C2C12 Myoblasts

Project description:ChIP-seq Profiling of RXRα in Proliferating C2C12 Myoblasts

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Transcriptional profiling of PRDM2 Knock down vs.controlGFPsh proliferating C2C12 Myoblasts

Project description:Knockdown of PRDM2 led to precocious differentiation. To understand the molecular basis for this phenotype, we performed microaary analysis of growing myoblasts. Genes differentially regulated by PRDM2 knock down were reveraled by microarray analysis using NIA15K mouse chips. Control and knock down cells were grown in proliferating conditions

2015-06-30 | E-GEOD-58675 | biostudies-arrayexpress

RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

Project description:We previously identified C/EBPβ as an inhibitor of myogenic differentiation and a regulator of muscle satellite cell self-renewal. We found that C/EBPβ is regulated during the transition from proliferation to growth arrest in myoblasts and overexpression of C/EBPβ in myoblasts promotes cell growth arrest in vitro and improves engraftment of satellite cells into the stem cell niche in vivo. To identify the molecular mechanism by which C/EBPβ regulates myoblast proliferation and growth arrest, we performed RNA-seq on C/EBPβ-overexpressing myoblasts.

2020-12-18 | GSE152051 | GEO

Gene expression profiling of PRDM2 Knockdown in proliferating, quiescent and differentiating myoblasts

Project description:Gene expression profiling of PRDM2 Knockdown in proliferating, quiescent and differentiating myoblasts

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Profiling of transcriptional targets of Jak1 and Stat1 in proliferating and differentiating myoblasts

Project description:Profiling of transcriptional targets of Jak1 and Stat1 in proliferating and differentiating myoblasts

| PRJNA1090896 | ENA

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.

2015-04-10 | GSE67703 | GEO

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