E-PROT-41
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-41 | ExpressionAtlas | 2022-01-10
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-PROT-41-analysis-methods.tsv | Tabular | |||
| E-PROT-41-configuration.xml | Xml | |||
| E-PROT-41-factors.xml | Xml | |||
| E-PROT-41-zoomifications-log.tsv | Tabular | |||
| E-PROT-41.condensed-sdrf.tsv | Tabular |
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Project description:Clinical proteomics research is in part limited by the availability of clinical samples. However, large biobanks exist worldwide containing formalin-fixed and paraffin embedded samples and samples stored in RNAlater. The extraction of proteins for proteome analysis from samples prepared by either method has been demonstrated. However, the impact of the preservation method on the result of a quantitative proteome analysis remains largely uninvestigated. We, therefore, conducted a proteome analysis of human colon mucosal biopsies where the material had been preserved accordingly. Twenty-four colon mucosal biopsies were extracted from the sigmoideum by endoscopy from two participants. The biopsies were either directly-frozen, stabilized in RNAlater, or stabilized by formaldehyde fixation immediately or incubated for 30 min to simulate a clinical situation, followed by paraffin embedding. The impact of the preservation method on the result of a proteome analysis was characterized by high throughput gel free quantitative proteomics.
2017-04-01 | MSV000080863 | MassIVE
Project description:Clinical proteomics research is in part limited by the availability of clinical samples. However, large biobanks exist worldwide containing formalin-fixed and paraffin embedded samples and samples stored in RNAlater. The extraction of proteins for proteome analysis from samples prepared by either method has been demonstrated. However, the impact of the preservation method on the result of a quantitative proteome analysis remains largely uninvestigated. We, therefore, conducted a proteome analysis of human colon mucosal biopsies where the material had been preserved accordingly. Twenty-four colon mucosal biopsies were extracted from the sigmoideum by endoscopy from two participants. The biopsies were either directly-frozen, stabilized in RNAlater, or stabilized by formaldehyde fixation immediately or incubated for 30 min to simulate a clinical situation, followed by paraffin embedding. The impact of the preservation method on the result of a proteome analysis was characterized by high throughput gel free quantitative proteomics.
2015-11-23 | PXD002029 | Pride
Project description:Microarrays were used to analyze the gene expression in endoscopic-derived intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) and controls Mucosal biopsies were obtained at endoscopy from the colon of 97 ulcerative colitis (UC), 8 Crohn's disease (CD) patients and 11 controls. The biopsies were taken at the most affected sites but at a distance of ulcerations. Disease activity was endoscopically assessed. Total RNA extracted from mucosal biopsies was used to analyze mRNA expression via Affymetrix Human Gene 1.0 ST arrays
2015-05-27 | E-GEOD-59071 | biostudies-arrayexpress
Project description:Background & Aims: Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state. Methods: Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and with irritable bowel syndrome (controls, n=10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden). Results: A clear separation between active UC, quiescent UC and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines revealing a plausible explanation to the abnormal regulated innate immune response seen in patients with UC. Conclusion: This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Keywords: Colonocytes, continuous inflammation, mucosal colonic biopsies, gene expression profiles Adjacent mucosal colonic biopsies were attained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and in controls (n=10). After extraction of total RNA, genome-wide gene expression data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Amplification was required to obtain sufficient amounts of labelled complementary RNA (cRNA) target for analysis with arrays. Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden).
2009-09-16 | E-GEOD-13367 | biostudies-arrayexpress
Project description:Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. This study aims at the characterisation of pathomechanisms and signalling in Campylobacter-induced diarrhoea in the human mucosa. During routine colonoscopy, biopsies were taken from patients suffering from campylobacteriosis. RNA-seq of colon biopsies was performed to describe Campylobacter jejuni-mediated effects. Mucosal mRNA profiles of acutely infected patients and healthy controls were generated by deep sequencing using Illumina HiSeq 2500. This data provide the basis for subsequent upstream regulator analysis.
2017-10-10 | GSE88710 | GEO
Project description:Background and aims: Mucosal abnormalities are potentially important in the primary pathogenesis of ulcerative colitis (UC). We investigated the mucosal transcriptomic expression profiles of biopsies from patients with UC and healthy controls (HC), taken from macroscopically non-inflamed tissue from the terminal ileum and three colonic locations with the objective of identifying abnormal molecules that might be involved in disease development. Methods: Whole-genome transcriptional analysis was performed on intestinal biopsies taken from 24 UC, 26 HC and 14 patients with CrohnM-bM-^@M-^Ys disease. Differential gene expression analysis was performed at each tissue location separately and results were then meta-analysed using FisherM-bM-^@M-^Ys method. Significantly differentially expressed genes were validated using qPCR. Gene location within the colon was determined using immunohistochemistry, subcellular fractionation, electron and confocal microscopy. DNA methylation was quantified by pyrosequencing. Results: Seven probes were abnormally expressed throughout the colon in UC patients with Family with sequence similarity member 5 C (FAM5C) being the most significantly underexpressed. Attenuated expression of FAM5C in UC was independent of inflammation, unrelated to phenotype or treatment, and remained low at rebiopsy approximately 23 months later. FAM5C is localised to the brush border of the colonic epithelium and expression is influenced by DNA methylation within its promoter. Conclusion: Genome-wide expression analysis of non-inflamed mucosal biopsies from UC patients identified FAM5C as significantly under-expressed throughout the colon in a major sub-set of patients with UC. Low levels of this gene could predispose to or contribute to the maintenance of the characteristic mucosal inflammation seen in this condition. Total RNA was extracted from the intestinal biopsies taken from macroscopically normal mucosa in the rectum, descending colon, ascending colon and terminal ileum in clinically quiescent Ulcerative colitis and Crohn's disease patients and compared to healthy controls. Normalized data for 26,261 probes out of 47,323 only. Criteria for inclusion not specified. The non-normalized matrix contains the complete non-normalized data for all probes.
2014-09-05 | E-GEOD-48634 | biostudies-arrayexpress
Project description:'Illumina Infinium HumanMethylation450 BeadChip data from CD326+ sorted colonic epithelial cells of mucosal biopsies from treatment-naive paediatric IBD patients (Crohn''s Disease or Ulcerative Colitis) or age-matched controls AC= ascending colon, PSC=sigmoid colon'
2015-09-15 | E-MTAB-3709 | biostudies-arrayexpress
Project description:Hypothesis: Gene expression differences in biopsies from patients with inflammatory bowel disease can be used to identify molecular heterogeneity within patients with active disease. Methods: Patients with a diagnosis of Crohn's disease, ulcerative colitis or normal healthy controls (with or without infectious colitis) underwent ileocolonoscopy. In healthy controls, biopsies were taken in the sigmoid colon (n=21), ascending/descending colon (n=25) and the terminal ileum (n=12). In patients with Crohn's disease, biopsies were taken in the ascending/descending colon (n=107) and terminal ileum (n=70) in uninflamed areas in all patients; in patients with mucosal lesions, additional biopsies were taken in inflamed regions of the ascending/descending colon (n=35) and terminal ileum (n=55). In ulcerative colitis patients, paired uninflamed sigmoid (n=48) and inflamed sigmoid biopsies (n=46) were taken. Biopsies were placed in RNAlater at the clinical site, frozen and shipped to Genentech, where they were disrupted using TissueLyzer beads, then RNA was isolated using RNeasy columns. RNA was hybridized to Agilent human 4x44kv1 arrays, dual channel, using universal reference.
2021-07-26 | GSE179285 | GEO
Project description:Background & Aims: Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state. Methods: Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n=8), quiescent UC (n=9), and with irritable bowel syndrome (controls, n=10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P11 software (Umetrics, Umeå, Sweden). Results: A clear separation between active UC, quiescent UC and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines revealing a plausible explanation to the abnormal regulated innate immune response seen in patients with UC. Conclusion: This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Keywords: Colonocytes, continuous inflammation, mucosal colonic biopsies, gene expression profiles
2009-09-16 | GSE13367 | GEO
Project description:Background and aims: Mucosal abnormalities are potentially important in the primary pathogenesis of ulcerative colitis (UC). We investigated the mucosal transcriptomic expression profiles of biopsies from patients with UC and healthy controls (HC), taken from macroscopically non-inflamed tissue from the terminal ileum and three colonic locations with the objective of identifying abnormal molecules that might be involved in disease development. Methods: Whole-genome transcriptional analysis was performed on intestinal biopsies taken from 24 UC, 26 HC and 14 patients with Crohn’s disease. Differential gene expression analysis was performed at each tissue location separately and results were then meta-analysed using Fisher’s method. Significantly differentially expressed genes were validated using qPCR. Gene location within the colon was determined using immunohistochemistry, subcellular fractionation, electron and confocal microscopy. DNA methylation was quantified by pyrosequencing. Results: Seven probes were abnormally expressed throughout the colon in UC patients with Family with sequence similarity member 5 C (FAM5C) being the most significantly underexpressed. Attenuated expression of FAM5C in UC was independent of inflammation, unrelated to phenotype or treatment, and remained low at rebiopsy approximately 23 months later. FAM5C is localised to the brush border of the colonic epithelium and expression is influenced by DNA methylation within its promoter. Conclusion: Genome-wide expression analysis of non-inflamed mucosal biopsies from UC patients identified FAM5C as significantly under-expressed throughout the colon in a major sub-set of patients with UC. Low levels of this gene could predispose to or contribute to the maintenance of the characteristic mucosal inflammation seen in this condition.
2014-09-05 | GSE48634 | GEO