Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of dexamethasone treatment on the transcriptome of injured mouse hamstring muscle

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE218699 | GEO | 2024/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression microarray analysis of whole mouse hamstring muscles to identify genes promoting the devlopment of neurogenic heterotopic ossifications following spinal cord injury

Project description:To better understand which genes/pathways are activated in injured muscles following a spinal cord injury (SCI) and how these promote the development of neurogenic heterotopic ossification (NHO), we performed gene expression profiling by microarray of muscles in the early phase following muscle injury.

2021-12-01 | GSE165062 | GEO

Effect of dexamethasone treatment on the transcriptome of injured mouse hamstring muscle

Project description:Effect of dexamethasone treatment on the transcriptome of injured mouse hamstring muscle

| PRJNA904909 | ENA

Real-time quantitative PCR analysis of microRNAs in a mice model of Neurogenic Heterotopic Ossifications (NHOs)

Project description:Neurogenic heterotopic ossifications are intramuscular bone formations developing following central nervous system injury. The pathophysiology is poorly understood and current treatments for this debilitating condition remain unsatisfying. Here we explored the role of miRNAs in a clinically relevant mouse model that combines muscle and spinal cord injury (SCI), and in patients’ cells. We found an osteo-suppressive miRNAs response in injured muscle that was hindered when the spinal cord injury was associated. In isolated fibro-adipogenic progenitors from damaged muscle (cells at the origin of ossification), spinal cord injury induced a downregulation of osteo-suppressive miRNAs while osteogenic markers were overexpressed. The overexpression of selected miRNAs in patient’s fibro-adipogenic progenitors inhibited mineralization and osteo-chondrogenic markers in vitro. Altogether, we highlighted an osteo-suppressive mechanism involving multiple miRNAs in response to muscle injury that prevents osteogenic commitment and which is ablated by the neurologic lesion in heterotopic ossification pathogenesis. This provides new research hypotheses for preventive treatments.

2023-09-20 | GSE241333 | GEO

Transcriptome responses to dexamethasone of the hypothalamus of pigs with different genotypes at the GRAla610Val mutation

Project description:The main aims of the experiment were to 1) chart gene networks governed by glucocorticoid receptor on a genome-wide scale, 2) to provide insights into mechanisms modulating glucocorticoid sensitivity and 3) to obtain better understanding of molecular and phenotypic consequences of the GRAla610Val substitution by examining its transcriptome signature in untreated and dexamethasone-treated animals. A total of 48 purebred German Landrace piglets were used in the experiment. At the time of the experiment the piglets were 7-weeks old. A bolus injection of either dexamethasone or sterile saline was administered intramuscularly into the neck muscle. Twenty piglets received saline, sixteen piglets were treated with 10 μg/kg dexamethasone, and twelve piglets were treated with 60 μg/kg dexamethasone. All three treatment groups were balanced for sex and genotype.

2021-11-30 | E-MTAB-7494 | biostudies-arrayexpress

Role of IL33 on muscle regneration in aging

Project description:We compare the effect of IL-33 vs PBS on muscle regneration from 22-month old mice 8 days post-injury. These analyses from whole muscle provide insight into the role of IL-33 on regeneration in the context of aging. The tibialis anterior muscle from male C57BL/6 mice (22 months old) were cryo-injured using a liquid nitrogen chilled metal probe for 8 seconds. Mice received 2 ug of rIL-33 via intraparitoneal injection the day prior and the day following cryoinjury. 8 days post-injury whole muscle was harvested and snap frozen in liquid nitrogen. Whole muscle was then homogenized directly in TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

2016-01-10 | E-GEOD-76695 | biostudies-arrayexpress

Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [ATAC]

Project description:Acute kidney injury (AKI) is a frequent and challenging clinical condition associated with high morbidity and mortality. In AKI, renal tubular epithelial cells (TECs) are a primary site of damage, and recovery from AKI depends on TEC plasticity. However, the molecular mechanisms underlying adaptation and maladaptation of TECs in AKI remain largely unclear. Here, our analyses of mouse kidney tubuloids showed that TEC injury resulted in activation of the glucocortiocoid receptor by endogenous glucocorticoids, which aggravated tubular damage. The detrimental effect of endogenous glucocorticoids on injured TECs was exacerbated by the administration of the widely clinically used synthetic glucocorticoid, dexamethasone, as indicated by experiments in mouse kidney tubuloids. Mechanistically, studies in mouse tubuloids demonstrated that glucocorticoid receptor signaling in injured TECs orchestrated a maladaptive transcriptional program to hinder DNA repair and to amplify injury-induced DNA double-strand break formation, as well as to dampen mTOR activity and mitochondrial bioenergetics. This study identifies glucocortiocoid receptor activation as a mechanism of epithelial maladaptation, which is functionally important for acute kidney injury.

2024-09-14 | GSE276041 | GEO

Glucocorticoids induce a maladaptive epithelial stress response to aggravate acute kidney injury [RNA]

2024-09-14 | GSE276040 | GEO

Interorgan communication in the neurogenic heterotopic ossification: focusing on the role of brain-derived extracellular vesicles

Project description:Brain-derived extracellular vesicles participate in inter-organ communication after traumatic brain injury by transporting pathogens to initiate secondary injury. Inflammasome related proteins encapsulated in brain-derived extracellular vesicles are capable of crossing the blood-brain barrier to reach distal tissues. These proteins initiate inflammatory dysfunction such as neurogenic heterotopic ossification. This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies. Accordingly, a rat model of neurogenic heterotopic ossification that combined traumatic brain injury and achillotenotomy was developed to address these two issues. Histological examination of the injured tendon identified the coexistence of ectopic calcification and fibroblast pyroptosis. The relationships among brain-derived extracellular vesicles, fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo. The present work highlighted the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offered a potential strategy for the prevention of neurogenic heterotopic ossification after traumatic brain injury.

2023-11-02 | PXD046626 |

Genome-wide profiling of muscle Treg cells from IL-33 treated mice

Project description:We report gene expression of Treg cells isolated from injured muscle in IL-33 vs PBS treated mice. Male Foxp3-GFP C57BL/6 reporter (2 months old) mice were injured intramuscularly with cardiotoxin/rIL-33 (0.3 ug/muscle). Tregs were sorted directly into Trizol from injured muscle 4 days post-injury. Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.

2016-01-12 | E-GEOD-76722 | biostudies-arrayexpress

Single-cell RNA sequencing of Ddr2 slie/slie and littermate control

Project description:Single-cell RNA sequencing was performed on injured and uninjured hindlimb tissue of Ddr2 slie/slie mice and littermate controls following 30% total body surface area burn and Achilles’ tenotomy injury to determine the role of DDR2 in heterotopic ossification and aberrant differentiation during wound healing.

2022-09-01 | GSE212281 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data