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Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [RNA-seq]

ABSTRACT: Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [RNA-seq]

PROVIDER: PRJNA897823 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22164768.fastq.gz	Fastqsanger.gz
	SRR22164769.fastq.gz	Fastqsanger.gz
	SRR22164770.fastq.gz	Fastqsanger.gz
	SRR22164771.fastq.gz	Fastqsanger.gz
	SRR22164772.fastq.gz	Fastqsanger.gz

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Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease

Project description:Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease

| PRJNA897821 | ENA

Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [Array]

Project description:Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [Array]

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Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease

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

2024-09-03 | GSE217164 | GEO

Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [Array]

Project description:Creeping fat, also known as mesenteric fat, which is connected to the inflamed segments of the intestine and is a hallmark of Crohn's disease (CD), appears to be correlated with disease activity. Adipose-stem cells isolated from the creeping fat of CD subjects were found to be dysfunctional (exhibiting a high inflammatory profile, high invasive and phagocytic capacities, and worse immunosuppressive properties), and this dysfunction persisted in hASCs taken from CD subjects who were in remission of the disease. We hypothesized that the abnormal behavior of adipose stem cells is caused by the accumulation of epigenetic modifications due to the inflammatory environment underlying active CD. DNA methylation and transcriptomics were performed in adipose-derived stem cells (ASCs) isolated from visceral adipose tissue biopsies of active and inactive CD patients and non-IBD patients. An integrative analysis of both omics was performed to obtain the best gene candidates.

2024-09-03 | GSE217124 | GEO

Integrative genome-wide DNA methylome and transcriptome data reveals key genes involved in the dysregulation of adipose-stem cells linked to Crohn’s disease [RNA-seq]

2024-09-03 | GSE217163 | GEO

Integration of genome-wide DNA methylome and transcriptome of human intestinal fibroblasts reveals novel candidate gene signatures in Crohn’s disease-associated fibrosis

Project description:Tissue fibrosis is a serious complication of Crohn’s disease (CD) as well as of a variety of other complex, chronic pathologies. Understanding the underlying pathophysiology of tissue fibrosis is crucial for the development of tissue-specific prevention and interventional treatment strategies. To identify molecular states specific to fibrotic disease, we employed deep sequencing to define the genome-wide DNA methylome and the whole transcriptome of purified human intestinal fibrotic fibroblasts (HIFs) isolated from the colon of patients with fibrotic CD. Integration of this information, via computational tools, identified candidate molecular interactions that could lead to fibrosis pathology. Our definition of a genome-wide fibrosis-specific DNA methylome provides a new paradigm for understanding mechanisms of pathological gene expression that lead to intestinal fibrosis and may have relevance to fibrogenesis in other organs.

2016-03-22 | GSE67250 | GEO

Blood-Derived DNA Methylation Signatures of Crohn’s Disease and Severity of Intestinal Inflammation

Project description:Crohn’s disease is a relapsing inflammatory disorder with a variable clinical course. While most patients present with purely an inflammatory phenotype (B1) at diagnosis, a subgroup (~20%) rapidly progresses to complicated disease manifestations that include stricturing (B2) within 5 years. DNA methylation is a key epigenetic mechanism that can regulate gene expression and thereby influence the development and progression of complex diseases. Site-specific DNA methylation differences have been reported in peripheral blood of patients with Crohn’s disease, but investigation of the temporal relationship between methylation and disease is required to establish whether the methylome plays a causal role and can be leveraged for therapeutic benefits. To this end, we conducted an epigenome-wide study of methylation (~850K sites) in peripheral blood at diagnosis and during follow-up from the RISK pediatric Crohn’s disease inception cohort. While some methylation changes associated with Crohn’s disease might be causal, in peripheral blood the vast majority are found to be a transient consequence of inflammation and thus a symptom of disease.

2018-04-03 | GSE112611 | GEO

Promoter methylome and integrative transcriptome profiling identify key epigenetics-regulated genes in human HCCs [methylation]

Project description:Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide and has a poor prognosis. Promoters represent an essential regulatory element of gene transcription in the human genome. In order to understand the promoter methylation in relation with gene transcription in HCCs, we applied a liquid hybridization capture-based bisulfite sequencing (LHC-BS) approach to examine the promoter methylome of HCCs, for which we customized 150,407 capture probes and enabled coverage of 91.8% of the RefSeq gene promoters within the human genome. We found the differential promoter DNA methylation between HCCs and peripheral normal tissues. Then we integrated promoter methylomic and transcriptomic profiling and described gene expression and regulation in HCCs. Lastly, we validated the key genes in a larger number of samples and screened candidate genes aberrantly regulated by DNA methylation in human HCCs. Capture-based whole genome promoter bisulfite-seq for 8 pairs of HCC tumor and non-tumor liver (NTL) samples.

2014-07-01 | E-GEOD-55752 | biostudies-arrayexpress

DNA methylome and transcriptome profiling reveal key electrophysiology and immune dysregulation in hypertrophic cardiomyopathy.

Project description:Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease. However, a detailed DNA methylation (DNAme) landscape has not yet been elucidated. Our study combined DNAme and transcriptome profiles for HCM myocardium and identify aberrant DNAme associated with altered myocardial function in HCM. The transcription of methylation-related genes did not significantly differ between HCM and normal myocardium. Nevertheless, the former had an altered DNAme profile compared with the latter. The hypermethylated and hypomethylated sites in HCM tissues had chromosomal distributions and functional enrichment of correlated genes differing from those of their normal tissue counterparts. The GO analysis of network underlying the genes correlated with DNAme alteration and differentially expressed genes (DEGs) shows functional clusters centred on immune cell function and muscle system processes. In KEGG analysis, only the calcium signalling pathway was enriched either by the genes correlated with changes in DNAme or DEGs. The protein-protein interactions (PPI) underlying the genes altered at both the DNAme and transcriptional highlighted two important functional clusters. One of these was related to the immune response and had the estrogen receptor-encoding ESR1 gene as its node. The other cluster comprised cardiac electrophysiology-related genes. Intelliectin-1 (ITLN1), a component of the innate immune system, was transcriptionally downregulated in HCM and had a hypermethylated site within 1500 bp upstream of the ITLN1 transcription start site. Estimates of immune infiltration demonstrated a relative decline in immune cell population diversity in HCM. A combination of DNAme and transcriptome profiles may help identify and develop new therapeutic targets for HCM.

| S-EPMC10072074 | biostudies-literature

Promoter methylome and integrative transcriptome profiling identify key epigenetics-regulated genes in human HCCs [expression]

Project description:Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide and has a poor prognosis. Promoters represent an essential regulatory element of gene transcription in human genome. In order to understand the promoter methylation in relation with gene transcription in HCCs, We applied a liquid hybridization capture-based bisulfite sequencing (LHC-BS) approach to examine the promoter methylome of HCCs, for which we customized 150,407 capture probes and enabled coverage of 91.8% of the RefSeq gene promoters within human genome. We found the differential promoter DNA methylation between HCCs and peripheral normal tissues. Then we integrated promoter methylomic and transcriptomic profiling and described gene expression and regulation in HCCs. Lastly, We validated the key genes in larger number of samples and screened candidate genes aberrantly regulated by DNA methylation in human HCCs.

2014-07-01 | GSE55758 | GEO

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