Effect of dexamethasone treatment on the transcriptome of injured mouse hamstring muscle
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA904909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22401840.fastq.gz | Fastqsanger.gz | |||
| SRR22401841.fastq.gz | Fastqsanger.gz | |||
| SRR22401842.fastq.gz | Fastqsanger.gz | |||
| SRR22401843.fastq.gz | Fastqsanger.gz | |||
| SRR22401844.fastq.gz | Fastqsanger.gz |
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Project description:Healthy muscle heals and repairs after injury. However, when mice are treated with dexamethasone, an agonist of glucocorticoid receptors, heterotopic ossifications (HO) develop in the injured muscle within fibrotic areas that fail to fully regenerate functional muscle. To understand the mechanisms driving heterotopic ossification in response to glucocorticoid receptor agonists, we performed RNA seqencing analysis on injured muscle. Mice underwent muscle injuries by intramuscular injection of cardiotoxin (CDTX). All mice were treated with either vehicle or dexamethasone (10mg/kg, intraperitoneal injection) daily from day 0-4. polyA+ RNA was isolated from whole muscle 4 days post injury, libraries generated and sequenced.
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Project description:A phenotypically and functionally distinct population of CD4+ Foxp3+ T cells (Tregs) rapidly accumulates in acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switch from a pro-inflammatory to a pro-regenerative state. Analysis of gene expression of Tregs and CD4+Foxp3- T cells (Tconvs) from injured muscle and spleen revealed that the transcriptome of muscle Treg cells is distinct from that of splenic Tregs. A set of genes is uniquely expressed by muscle Tregs, while another set is over-expressed by the two muscle populations vis-à-vis their two spleen counterparts. 6 wk-old Foxp3-ires-GFP mice were injured in skeletal muscles with cardiotoxin. Four and fourteen days later, Tregs and Tconvs from spleen and muscle were double-sorted into Trizol. To reduce variability, cells from multiple mice were pooled for sorting, and three replicates were generated for all groups. RNA from 1.5-2.5 x 104 cells was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.
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Project description:Context: Glucocorticoids are frequently prescribed drugs with important side-effects such as glucose intolerance and tissue remodelling. Objective: The goal was to explore the molecular basis of the crosstalk between adipose tissue and skeletal muscle during short term glucocorticoid treatment. Design and Intervention: Healthy male subjects were assigned to a 4-d treatment with dexamethasone at 4mg/d. Main Outcome Measures: Primary outcome measures were gene expression profiling of adipose tissue and skeletal muscle. Urinary cortisol and metabolic biochemistry were also assessed. Dexamethasone was provided in 0.5 mg tablets as 4mg per day during 4 days to male healthy volunteers. Skeletal muscle and adipose tissue biopsies were obtained at the beginning and at the end of the protocol. The transcriptome analysis compared before vs. after the 4 days dexamethasone treatment using a dye swap design and whole genome 4x44k oligonucleotide arrays (Agilent Technologies).
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Project description:Analysis of dexamethasone-regulation of muscle mass at gene expression level. The hypothesis tested in the present study was that the presence of MuRF1 contributes to the extent of gene expression changes observed in specific sets of genes during a challenge leading to muscle atrophy. Results provide important information on the response of triceps surae muscle to synthetic glucocorticoid treatment, such as specific cell signaling and metabolic enzyme genes, that may be influenced by MuRF1 during atrophy. Total RNA obtained from isolated triceps surae muscle subjected to 3 or 14 days dexamethasone treatment compated to untreated littermate control muscles.
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