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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

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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 [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 [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.

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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]

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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.

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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.

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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.

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