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MiR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies

ABSTRACT: miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies

PROVIDER: PRJNA740321 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14416844_1.fastq.gz	Fastqsanger.gz
	SRR14416844_2.fastq.gz	Fastqsanger.gz
	SRR14416845_1.fastq.gz	Fastqsanger.gz
	SRR14416845_2.fastq.gz	Fastqsanger.gz
	SRR14416846_1.fastq.gz	Fastqsanger.gz

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MicroRNA-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [eCLIP-seq]

Project description:Duchenne muscular dystrophy (DMD) is an X-linked progressive muscle disorder resulting in muscle weakness and cardiomyopathy. MicroRNAs have shown to play a significant role in muscle development, metabolism, and disease pathologies. We demonstrated that miR-486 expression is reduced in DMD muscles and its expression levels correlate with dystrophic disease severity. miR-486 knockout mice developed disrupted myofiber architecture, decreased myofiber size, decreased locomotor activity, increased fibrosis, and metabolic defects that were exacerbated on the dystrophic mdx5cv background. We integrated RNA-sequencing and chimeric eCLIP-sequencing data to identify direct in vivo targets of miR-486 and associated dysregulated gene signatures in skeletal muscle. Together, our studies identify miR-486 as a driver of muscle remodeling in DMD, a useful biomarker for dystrophic disease progression, and highlight chimeric eCLIP-sequencing as a useful tool to identify direct in vivo microRNA target transcripts.

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miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [RNA-seq]

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MicroRNA-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [eCLIP-seq]

Project description:MicroRNA-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [eCLIP-seq]

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miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [RNA-seq]

Project description:miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [RNA-seq]

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miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies

Project description:This SuperSeries is composed of the SubSeries listed below.

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Atrogin-1 regulates BiP levels - novel therapeutic targets for Duchenne Muscular Dystrophy

Project description:Skeletal muscle wasting results from numerous pathological conditions impacting both the musculoskeletal and nervous systems. A unifying feature of these pathologies is the upregulation of members of the E3 ubiquitin ligase family, resulting in increased proteolytic degradation of target proteins. Despite the critical role E3 ubiquitin ligases in regulating muscle mass, the specific proteins they target for degradation and the mechanisms by which they regulate skeletal muscle homeostasis remain ill-defined. Here, using zebrafish loss of function models combined with in vivo cell biology and proteomic approaches, we identified the endoplasmic reticulum chaperone, BiP, as a novel target of the E3 ubiquitin ligase atrogin-1. A loss in atrogin-1 results in an accumulation of BiP, leading to impaired mitochondrial dynamics and a subsequent loss in muscle fibre integrity. We further implicate a disruption in atrogin-1 mediated BiP regulation in the pathogenesis of Duchenne Muscular Dystrophy. We reveal that BiP is not only upregulated in Duchenne Muscular Dystrophy, but its inhibition using pharmacological strategies, or by upregulating atrogin-1, significantly ameliorates pathology in a zebrafish model of Duchenne Muscular Dystrophy. Collectively, our data implicates a novel disease axis in the pathogenesis of Duchenne Muscular Dystrophy, and highlights atrogin-1’s essential role in maintaining muscle homeostasis.

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Genetic Modifiers of Duchenne Muscular Dystrophy

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Project description:Large animal models for Duchenne muscular dystrophy (DMD) are indispensible for preclinical evaluation of novel diagnostic procedures and treatment strategies. To evaluate functional consequences of Duchenne muscular dystrophy (DMD) in skeletal muscle and myocardium, we used a new genetically engineered dystrophin KO pig model displaying hallmarks of human DMD. Heart and skeletal muscle tissue samples of DMD pigs and wild-type (WT) controls at three different ages were analyzed by label-free proteomics.

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Gene expression data from Duchenne muscular dystrophy patients versus controls

Project description:gene expression data is from RNA extracted from muscle biopsy samples taken from boys with Duchenne muscular dystrophy (DMD) or pathologically normal controls (CTRL). Each muscle biospy was examined in detail histologically by Dr. Eric P. Hoffman at Children's National Medical Center to determine stage of disease. In addition, the absence or presence of dystrophin was determined via western blot analyses. We utilized Human U133 2.0 arrays to examine the transcriptome of each muscle, and then we compared differential gene expression between DMD patient muscles and CTRL muscules. We set the FDR p value for significance at 0.05 and at least a 1.5 fold difference in DMD/CTRL compared differential gene exrpression between DMD versus Control

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