Similar Datasets
Project description:Colon gene expression in human IBD. The three major clinical subsets of Inflammatory Bowel Disease (IBD) include colon-only Crohn's Disease (CD), ileo-colonic CD, and Ulcerative Colitis (UC). These experiments tested differential colon gene expression in these three types of IBD, relative to healthy control samples, and the local degree of mucosal inflammation as measured by the CD Histological Index of Severity (CDHIS). Colon biopsy samples were obtained from IBD patients at diagnosis and during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, with a focus upon candidate genes identified in a recent genome wide association study in pediatric onset IBD. Data suggested that two of these candidate genes are up regulated in pediatric IBD, partially influenced by local mucosal inflammation. These experiments tested differential colon gene expression in healthy, CD, and UC samples for candidate genes identified in a recent pediatric onset IBD genome wide association study. Keywords: Single time point in CD and UC and healthy controls.
2009-03-11 | GSE10616 | GEO
Project description:Reference-guided genome assembly of long non-coding RNA transcripts reveals target genes associated with Crohn’s disease
| PRJNA1414275 | ENA
Project description:Crohn’s disease (CD) is a subtype of inflammatory bowel disease (IBD) characterized by transmural disease. The concept of transmural healing (TH) has been proposed as an indicator of deep clinical remission of CD and as a predictor of favorable treatment endpoints. Understanding the pathophysiology involved in transmural disease is critical to achieving these endpoints. How-ever, most studies have focused on the colon intestinal mucosa, overlooking the contribution of the colon intestinal wall in Crohn’s disease. Multi-omics approaches have provided new avenues for exploring the pathogenesis of Crohn’s disease and identifying potential biomarkers. Therefore, we analyzed and compared the gene and protein expression and dysregulated biological functions in the distinct tissue compartments of mucosa and submucosa/wall of colon resections from CD patients. We aimed to use transcriptomic and proteomic technologies to compare immune and mesenchymal cell profiles and pathways in the mucosal and submucosa/wall compartments to better understand refractory disease elements to achieve transmural healing. We employed a comprehensive multi-omics approach to investi-gate the molecular profiles of the colon mucosa and submucosa/wall compartments in patients with chronic Crohn’s disease. The results revealed similarities and differences in gene and protein ex-pression profiles, metabolic mechanisms, and immune and non-immune pathways between these two compartments. Additionally, the identification of protein isoforms highlights the complex molecular mechanisms underlying this disease. These findings have the potential to inform the development of novel therapeutic strategies to achieve TH.
2024-06-23 | PXD050335 | Pride
Project description:Colon gene expression in human IBD. The three major clinical subsets of Inflammatory Bowel Disease (IBD) include colon-only Crohn's Disease (CD), ileo-colonic CD, and Ulcerative Colitis (UC). These experiments tested differential colon gene expression in these three types of IBD, relative to healthy control samples, and the local degree of mucosal inflammation as measured by the CD Histological Index of Severity (CDHIS). Colon biopsy samples were obtained from IBD patients at diagnosis and during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, with a focus upon candidate genes identified in a recent genome wide association study in pediatric onset IBD. Data suggested that two of these candidate genes are up regulated in pediatric IBD, partially influenced by local mucosal inflammation. These experiments tested differential colon gene expression in healthy, CD, and UC samples for candidate genes identified in a recent pediatric onset IBD genome wide association study. Keywords: Single time point in CD and UC and healthy controls. Colon RNA was isolated from biopsies obtained from CD and UC at diagnosis and during therapy and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1,2,3,4,5) used for normalization of the Sample VALUEs are also contained within this data set.
2009-03-10 | E-GEOD-10616 | biostudies-arrayexpress
Project description:Altered function of the intestinal epithelium has been considered to play a key role in CD pathogenesis, however exact mechanisms that contribute towards lifelong relapsing mucosal inflammation remain ill defined. DNA methylation (DNAm) is a key epigenetic mechanism known to determine cellular identity by regulating gene transcription with alterations increasingly being implicated in IBD pathogenesis. We generated 312 intestinal epithelial organoids (IEOs) from mucosal stem cells obtained from 168 patients diagnosed with CD, non-IBD/healthy controls and Ulcerative colitis (UC). Genome wide epigenetic profiling of IEOs and primary purified epithelium revealed highly stable, CD associated loss of DNAm in MHC-I related genes which correlated with increased gene expression. Related Single Cell Portal accession number: SCP1884 Related Gene Expression Omnibus accession numbers: GSE57945, GSE75214
2024-03-31 | E-MTAB-12841 | biostudies-arrayexpress
Project description:Inflammatory bowel disease (IBD) is known to be caused by a genetic predisposition involving multiple genes; however, there is growing evidence that abnormal interaction with environmental, particularly epigenetic, factors can have a significant contribution during the development of IBD. Although many studies, particularly genome-wide association studies (GWAS), have been performed to identify the genetic changes underlying the pathogenesis of Crohn’s disease (CD), the role of epigenetic changes in the development of complications arising from CD is poorly understood. Here, we employed an unbiased approach to define DNA methylation alteration in CD patients using the HumanMethylation450K BeadChip platform. Compared to normal controls, the majority of differential DNA methylation in CD patient samples was in the promoter, intergenic, and gene body regions. The DNA methylation profile in CD revealed 134 probes (23 hypermethylated and 111 hypomethylated probes) that were differentially methylated. We validated the methylation levels of 19 genes that showed hypermethylation in CD patients compared with normal control. Technical validation was performed using quantitative MSP analysis and we finally identified that the Fragile Histidine Triad (FHIT) genes were hypermethylated in a disease-specific manner. Gene network analysis of the hypermethylated candidates suggested putative molecular interactions relevant to IBD pathology. Overall, our DNA methylation profile identifies newly hypermethylated genes in CD, as well as the gene network associated with disease development, which can provide new therapeutic targets.
2017-12-25 | GSE105798 | GEO
Project description:Activation of inflammatory pathways in human IBD IL-6:STAT3 pathways are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory IL-6:STAT3 dependent networks would be up regulated in the colon of pediatric patients with Crohn Disease (CD) and Ulcerative Colitis (UC), and that these would regulate leukocyte survival, proliferation, and recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy, CD, and UC samples. Colon biopsy samples were obtained from CD and UC patients at diagnosis, CD patients during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that two IL-6:STAT3 dependent networks are up regulated in pediatric IBD both at diagnosis and during therapy which regulate leukocyte recruitment and survival. The degree of up regulation of these genes compared to healthy controls was remarkably conserved across the two CD groups and the UC groups, suggesting common mechanisms of mucosal inflammation. Keywords: Single time point in CD, UC, and healthy controls.
2008-01-01 | GSE9686 | GEO
Project description:Activation of inflammatory pathways in human IBD IL-6:STAT3 pathways are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory IL-6:STAT3 dependent networks would be up regulated in the colon of pediatric patients with Crohn Disease (CD) and Ulcerative Colitis (UC), and that these would regulate leukocyte survival, proliferation, and recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy, CD, and UC samples. Colon biopsy samples were obtained from CD and UC patients at diagnosis, CD patients during therapy, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that two IL-6:STAT3 dependent networks are up regulated in pediatric IBD both at diagnosis and during therapy which regulate leukocyte recruitment and survival. The degree of up regulation of these genes compared to healthy controls was remarkably conserved across the two CD groups and the UC groups, suggesting common mechanisms of mucosal inflammation. Colon RNA was isolated from biopsies obtained from CD at diagnosis and during therapy, UC at diagnosis, and healthy controls. Samples were obtained from the most proximal affected segment of colon. Microarray experiments were performed as described in the CCHMC microarray core, and data was analyzed as described above in the summary. The '107' internal control CEL files (for batches 1-4) used for normalization of the Sample VALUEs are linked below as supplementary files.
2010-05-27 | E-GEOD-9686 | biostudies-arrayexpress
Project description:To investigate the mechanism of demethylase FTO in Crohn's disease，We used RNA-seq data from three normal colon samples and three TNBS-induced IBD colon samples of C57 mice for gene expression profiling.
2025-11-09 | GSE280244 | GEO
Project description:To interrogate the potential of αEβ7 integrin as a target in Crohn’s disease (CD), we single cell RNA-sequenced T cells from a patient with CD and a non-IBD control
2023-12-28 | GSE252122 | GEO