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A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease

ABSTRACT: A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease

PROVIDER: PRJNA801001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17774818_1.fastq.gz	Fastqsanger.gz
	SRR17774818_2.fastq.gz	Fastqsanger.gz
	SRR17774819_1.fastq.gz	Fastqsanger.gz
	SRR17774819_2.fastq.gz	Fastqsanger.gz
	SRR17774820_1.fastq.gz	Fastqsanger.gz

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A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease [array]

Project description:A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease [array]

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A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease [scRNA-Seq]

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A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease [array]

Project description:The intestinal epithelium is a single-cell layer comprising a constellation of specialized cell types that functionally interconnect host physiological systems with extrinsic microbial communities, metabolites, and dietary factors1. Active renewal of the intestinal epithelium relies on stem cells that reside in invaginations of the epithelium known as crypts. Inflammatory Bowel Disease (IBD) disrupts normal functions and/or proportions of cells in the intestinal epithelium, including stem cell programming during epithelial restitution. Genome-wide association studies have provided a powerful means to identify loci and genes contributing to IBD risk and functional annotation of candidate genes have unveiled cellular programs and molecular mechanisms involved in IBD etiology. Here we find that risk for a major form of IBD, Crohn’s disease (CD), is linked to a variant of the Fibroblast Growth Factor Receptor 1 Oncogene Partner (FGFR1OP) locus, which encodes a protein of the centrosome, the microtubule organizing center that generates microtubule structures involved in cell division, polarity, and motility. Deletion of Fgfr1op in mouse intestinal epithelium impaired stem cell division and intestinal crypt architecture causing crypt loss, inflammation and death. Transcriptional, biochemical and morphological analyses demonstrated that Fgfr1op coordinates the centrosome with the actin cytoskeleton and with specialized cell junctions known as desmosomes. We conclude that a genetically inherited centrosomal defect predisposes to CD by affecting renewal of the intestinal epithelium.

2024-06-17 | GSE194311 | GEO

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A centrosomal defect of intestinal stem cells predisposes to Crohn’s Disease

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

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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.

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Project description:This RNA seq experiment was designed to identify a gene signature of a CCR5-expressing subset of human intestinal Th17-cells. T helper-cells from peripheral blood of healthy donors and from the lamina propria of Crohn’s Disease patients were FACS-purified according to the expression of the chemokine receptors CCR6, CCR5 and CXCR3. Four CCR6+Th- subsets were isolated according to CXCR3 and CCR5 expression: two CXCR3- Th17 subsets (CCR5-: “cTh17” or CCR5+: “pTh17”) and two subsets of CXCR3+ Th1/17-cells (CCR5+ or CCR5-)

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