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Muscle injury causes gene expression changes that are related to long-term changes in stem cell DNA methylation [RNA-Seq]

ABSTRACT: Muscle injury causes gene expression changes that are related to long-term changes in stem cell DNA methylation [RNA-Seq]

PROVIDER: PRJNA595926 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10704063.fastq.gz	Fastqsanger.gz
	SRR10704064.fastq.gz	Fastqsanger.gz
	SRR10704065.fastq.gz	Fastqsanger.gz
	SRR10704066.fastq.gz	Fastqsanger.gz
	SRR10704067.fastq.gz	Fastqsanger.gz

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Muscle injury causes long-term changes in stem cell DNA methylation [RRBS]

Project description:Muscle injury causes long-term changes in stem cell DNA methylation [RRBS]

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Muscle injury causes gene expression changes that are related to long-term changes in stem cell DNA methylation [RNA-Seq]

Project description:Injury to muscle brings about the activation of stem cells, which then generate new myocytes to replace the damaged tissue. We now demonstrate that this activation causes a dramatic change in the stem cell methylation pattern that prepares them epigenetically for terminal myocyte differentiation. These demethylation and de novo methylation events occur at regulatory elements associated with genes involved in myogenesis. Local injury of one muscle brings about an almost identical epigenetic change in satellite cells from other muscles in the body, as well. Furthermore, this same methylation state is also generated in muscle stem cells of female animals following full-term pregnancy, even in the absence of any injury. In all of these cases, which appear to be mediated by circulating factors, the new methylation profile is then stably maintained in resident muscle stem cells and thus represents a molecular memory of previous physiological events that is probably programmed to provide a mechanism for adapting to the environment. Here we show the changes in gene expression that accompany the changes in DNA methylation.

2022-12-01 | GSE142111 | GEO

Muscle injury causes long-term changes in stem cell DNA methylation [RRBS]

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Muscle injury causes long-term changes in stem-cell DNA methylation.

Project description:Injury to muscle brings about the activation of stem cells, which then generate new myocytes to replace damaged tissue. We demonstrate that this activation is accompanied by a dramatic change in the stem-cell methylation pattern that prepares them epigenetically for terminal myocyte differentiation. These de- and de novo methylation events occur at regulatory elements associated with genes involved in myogenesis and are necessary for activation and regeneration. Local injury of one muscle elicits an almost identical epigenetic change in satellite cells from other muscles in the body, in a process mediated by circulating factors. Furthermore, this same methylation state is also generated in muscle stem cells (MuSCs) of female animals following pregnancy, even in the absence of any injury. Unlike the activation-induced expression changes, which are transient, the induced methylation profile is stably maintained in resident MuSCs and thus represents a molecular memory of previous physiological events that is probably programmed to provide a mechanism for long-term adaptation.

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Muscle injury prepares stem cells for terminal myocyte differentiation through changes in gene expression and long-term changes in DNA methylation

Project description:Muscle injury prepares stem cells for terminal myocyte differentiation through changes in gene expression and long-term changes in DNA methylation

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Microglia adopt longitudinal transcriptional changes after traumatic brain injury

Project description:Traumatic brain injury (TBI) is an under-recognizedpublic healththreat. Even mild brain injuries can lead to long-term neurologic impairment.Microgliaplay a fundamental role in the development and progression of this ensuing neurologic impairment. Despite this, a microglia-specific injury signature has yet to be identified. We hypothesized that TBI would lead to long-term changes in the transcriptional profile of microglial pathways associated with the development of subsequent neurologic impairment.

2023-12-11 | GSE249918 | GEO

Changes in Protein Fluxes and Gene Expression in Non-Injured Muscle Tissue Distant from an Acute Myotoxic Injury in Male Mice

Project description:The response to acute myotoxic injury requires stimulation of local repair mechanisms in the damaged tissue. However, satellite cells in muscle distant from acute injury have been reported to enter a functional state between quiescence and active proliferation. Here, we asked whether protein flux rates are altered in muscle distant from acute local myotoxic injury and how they compare to changes in gene expression from the same tissue. Broad and significant alterations in protein turnover were observed across the proteome in the limb contralateral to injury during the first 10 days after. Interestingly, mRNA changes had almost no correlation with directly measured protein turnover rates. In summary, we show consistent and striking changes in protein flux rates in muscle tissue contralateral to myotoxic injury, with no correlation between changes in mRNA levels and protein synthesis rates. This work motivates further investigation of the mechanisms, including potential neurologic factors, responsible for this distant effect.

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Mitochondrial perturbation in the intestine causes microbiota-dependent injury and gene signatures discriminative of inflammatory disease

Project description:Mitochondrial dysfunction is associated with inflammatory bowel diseases (IBD). To understand how microbial-metabolic circuits contribute to intestinal tissue injury, we disrupt mitochondrial function in the intestinal epithelium by deleting heat shock protein 60 (Hsp60Δ/ΔIEC). While metabolic perturbation causes self-resolving tissue injury, regeneration is disrupted in the absence of aryl hydrocarbon receptor (Hsp60Δ/ΔIEC;AhR-/-) or IL-10 (Hsp60Δ/ΔIEC;Il10-/-) leading to IBD-like pathology. Tissue pathology is absent in the distal colon of germfree (GF) Hsp60Δ/ΔIEC mice, highlighting bacterial control of metabolic injury. Selective colonization of GF Hsp60Δ/ΔIEC mice with the synthetic community OMM12 confirms expansion of metabolically-flexible Bacteroides ssp., which generates metabolic injury in mono-colonized mice. Transcriptional profiling of metabolically-impaired epithelium identifies gene signatures, such as Ido1, Nos2, and Duox2, differentiating active from inactive tissue inflammation in 343 tissue sections from Crohn’s disease patients. In conclusion, mitochondrial perturbation of the epithelium causes microbiota-dependent tissue injury and discriminative inflammatory gene profiles with relevance for IBD.

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Long-term consequences of chronic fluoxetine exposure on the expression of myelination-related genes in the rat hippocampus

Project description:To more concretely elucidate the long-term effects of chronic SSRI exposure during adulthood, the long-term consequences of chronic fluoxetine (12 mg/kg) versus vehicle treatment during adulthood (postnatal day (PND) 67-88) on gene expression in the hippocampus were investigated. The study showed that adult chronic fluoxetine exposure causes on the long-term changes in the expression of genes related to, amongst others, myelination

2016-01-22 | GSE67203 | GEO

Long-Term Gene Expression Dynamics at the Neurovascular Unit After Cerebral Ischemia/Reperfusion Injury in Mice

Project description:With increasing distribution of endovascular stroke therapies, transient middle cerebral artery occlusion in mice depicts a relevant patient population with recanalized M1 occlusion. This study provides a well-controlled transcriptome dataset of short and long-term transcriptomic changes at the neurovascular unit in cerebral ischemia/reperfusion injury.

2020-03-10 | GSE131193 | GEO