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Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics

ABSTRACT: Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics

PROVIDER: PRJNA813541 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18257300_1.fastq.gz	Fastqsanger.gz
	SRR18257300_2.fastq.gz	Fastqsanger.gz
	SRR18260300_1.fastq.gz	Fastqsanger.gz
	SRR18260300_2.fastq.gz	Fastqsanger.gz
	SRR18257301_1.fastq.gz	Fastqsanger.gz

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Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (scRNA-Seq).

Project description:Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (scRNA-Seq).

| PRJNA813543 | ENA

Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (RNA-Seq).

Project description:Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (RNA-Seq).

| PRJNA813544 | ENA

Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (scRNA-Seq).

Project description:The role of tissue resident macrophages during tissue regeneration or fibrosis is not well-understood, mainly due to the lack of a specific marker for their identification. Here, we identified two populations of skeletal muscle resident macrophages: TIM4- macrophages which are replenished from the blood and LYVE1+TIM4+ macrophages that locally self-renew (self-renewing resident macrophages, SRRMs). Using a CSF1R inhibition/withdrawal approach to specifically deplete SRRMs, we found that they provide a non-redundant function in clearing damage-induced apoptotic cells early after extensive acute injury. In contrast, in chronic mild injury as seen in a mouse model of Duchenne muscular dystrophy, we showed that depletion of both resident populations through long term CSF1R inhibition changes muscle fiber composition from damage-sensitive glycolytic fibers towards damage-resistant glycolytic-oxidative fibers protecting muscle against contraction induced injury. This later finding reveals a new role for resident macrophages in modulating tissue metabolism and has therapeutic potential in light of the ongoing clinical testing of CSF1R inhibitors.

2022-07-01 | GSE198055 | GEO

Metabolic reprogramming of skeletal muscle by resident macrophages points to CSF1R inhibitors as muscular dystrophy therapeutics (RNA-Seq).

2022-07-01 | GSE198054 | GEO

Mouse Models for Muscular Dystrophy

Project description:Comparative analysis of gene expression levels from hindlimb muscle tissue from 8 week old mouse models for muscular dystrophy. We have used mouse models with dystrophin-, sarcoglycan-, sarcospan-, or dysferlin-deficiency. Keywords = muscular dystrophy

2010-06-06 | E-GEOD-2112 | biostudies-arrayexpress

Mouse Models for Muscular Dystrophy

2005-11-24 | GSE2112 | GEO

Laminin-deficient muscular dystrophy, dy/dy diaphragm

Project description:Laminin (merosin) deficient muscular dystrophy in dy/dy mouse diaphragm muscle, 8 weeks old Keywords: muscle, muscular dystrophy, laminin, merosin, diaphragm, mouse

2006-03-16 | GSE3252 | GEO

fhl2b expression ameliorates muscular dystrophy

Project description:fhl2b expression ameliorates muscular dystrophy

| PRJNA1011837 | ENA

Transcription profiling of human Facioscapulohumeral muscular dystrophy (FSHD) muscle profiles

Project description:Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disorder linked to contractions of the D4Z4 repeat array in the subtelomeric region of chromosome 4q. By comparing genome-wide gene expression data from muscle biopsies of patients with FSHD to those of 11 other neuromuscular disorders, we intend to identify disease-specific changes which are more likely to be involved in the early stages of the disease progression. The data will help to identify pathological mechanisms involved in FSHD. Experiment Overall Design: Comparison of the profiles of FSHD to 13 other conditions for disease-specific changes. The 13 conditions are NHM (Normal healthy muscle) n=15; JDM (Juvenile dermatomyositis) n=25; HSP (Human spastic paraplegia) n=4; FSHD (facioscapulohumeral dystrophy) unaffected n=5, affected n=9; FKRP (Fukutin related protein deficiency) n=7; ED-L (Emery-Dreifuss muscular dystrophy, lamin A/C deficiency) n=4; ED-E (Emery-Dreifuss muscular dystrophy, emerin deficiency) n=4; DYSF (dysferlinopathy) n=10; DMD (Duchenne Muscular Dystrophy) n=10; CALP (Calpain-3 deficiency) n=10; BMD (Becker Muscular Dystrophy) n=5; AQM (Acute quadriplegic myopathy) n=5; ALS (Amyotrophic lateral sclerosis) n=9.

2008-06-16 | E-GEOD-9397 | biostudies-arrayexpress

Decoding the transcriptome of muscular dystrophy using single-nucleus RNA sequencing

Project description:Muscular dystrophy is a group of diseases that cause progressive weakness and degeneration of the skeletal muscles that control movement. Lacking polymerase I transcription release factor (PTRF, also known as Cavin1), an essential caveolae component, causes a secondary deficiency of caveolins resulting in muscular dystrophy. Because skeletal muscle is a heterogeneous tissue composed of different metabolic muscle fiber (myofibers) and mononuclear cells, the transcriptome responses of these myofibers and mononuclear cell to muscular dystrophy caused by PTRF deletion has not been explored. Here, we create muscular dystrophy mice caused by the deletion of PTRF gene and apply single-nucleus RNA sequencing (snRNA-seq) to unveil transcriptional changes in the skeletal muscle of mice with muscular dystrophy at single-nucleus resolution.

2023-05-31 | GSE217390 | GEO

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