Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic Analysis of Eosinophilic Esophagitis: Identification and Involvement of the Minichromosome Maintenance Complex as a Driver of Esophageal Basal Zone Hyperplasia

ABSTRACT: To uncover molecular drivers of Eosinophilic Esophagitis (EoE), a global proteome screen of the esophageal biopsies from individuals with and without EoE was performed.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Homo Sapiens (human)

DISEASE(S): Eosinophilic Esophagitis

SUBMITTER: Aleksandra Nita-Lazar

LAB HEAD: Aleksandra Nita-Lazar

PROVIDER: PXD040030 | Pride | 2023-08-01

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

The EoE esophageal epithelial transcriptomic landscape

Project description:We report alterations in the esophageal transcriptome of adult eosinophilic esophagitis (EoE) patients at a single-cell transcriptomic level.

2023-08-07 | GSE218607 | GEO

Potential proteins identification for stent restenosis induced by esophageal benign hyperplasia in esophageal cancer

Project description:This study was conducted to explore the potential proteins associated with esophagus benign hyperplasia induced by esophageal stents.

2023-03-10 | PXD014242 | Pride

IL-13 involvement in eosinophilic esophagitis: transcriptome analysis

Project description:3 eosinophilic esophagitis biopsies, cultured and stimulated with IL-13 : each of them was either left unstimulated or stimulated (100ng for 48h) We used microarray to uncover the IL-13-induced genes in esophageal epithelial cells of the esophagus Keywords: treated vs non treated

2007-12-21 | GSE8853 | GEO

Single-cell RNA Sequencing of Human Esophageal Epithelium in Homeostasis and Allergic Inflammation

Project description:To investigate gene expression signature of the human esophageal epithelium at the homeostatic and inflammatory conditions we performed scRNAseq on the human esophageal biopsies obtained from the healhy patients, patients with active eosinophilic esophagitis (EoE) and patients in the remission.

2022-06-15 | GSE201153 | GEO

Eosinophilic esophagitis-associated epithelial remodeling may limit esophageal carcinogenesis

Project description:Eosinophilic esophagitis and esophageal squamous cell carcinoma both feature epithelial remodeling in the form of hyperplasia. We used scRNA-Seq to examine the cellular and molecular alterations between these distinct pathologies.

2022-11-21 | GSE218118 | GEO

Generation of esophageal basal progeitor cells from human pluripotent stem cells

Project description:We established an efficient protocol to generate esophageal epithelial progenitors (EPCs) from human pluripotent stem cells (hPSCs). Inhibition of TGFß and BMP signaling is required for the differentiation of hPSCs into EPCs which can be further purified with EPCAM and Integrin ß4. These purified EPCs express human fetal esophageal genes and recapitulate the normal development of the stratified squamous epithelium. We performed global transcriptomic profiling of E12.5 mouse embryonic esophageal epithelia, human fetal esophageal epithelia and human embryonic stem cell RUES2-derived esophageal progenitor cells through RNA sequencing. We found that these cells shared similar expression of NOTCH components including Jag1 and 2, Dll1, 3 and 4, and Notct1, 3, 4. The gene expression profile allows to understand transcriptional program in mouse and human developing esophagus.

2018-08-31 | GSE116272 | GEO

Transcriptomic profiling of esophageal epithelium reveals enrichment of IFN-γ response gene signature during active EoE.

Project description:Eosinophilic esophagitis (EoE) is a chronic, allergic inflammatory disease of the esophageal mucosa. Although type 2 cytokines are predominant, targeting type 2 inflammation alone is not always effective for all patients. In EoE patients, the transcriptional profiling of esophageal biopsy reveals upregulation of type I and II interferon (IFN) response, dysregulated immune signaling, and downregulation of esophageal-specific genes. However, further investigation is needed to examine the gene expression changes in esophageal epithelium because it plays an important role in EoE. To investigate the upregulation of Interferon Stimulated Genes (ISGs) in EoE esophageal epithelium, we isolated epithelial cells from active EoE patients and non-EoE controls. We performed bulk RNA sequencing to analyze the epithelial-specific transcriptome in EoE. Unsupervised hierarchical clustering of the most variable genes differentiated the active EoE biopsies from non-EoE controls. Gene set enrichment analysis identified IFN-γ response as the most significant upregulated pathway.

2024-02-26 | GSE234973 | GEO

The minichromosome maintenance replicative helicase.

Project description: Not available

| S-EPMC3809582 | biostudies-literature

Effect of IFN-α and IFN-γ on gene expression of 3D organoids derived from telomerase-immortalized normal human esophageal keratinocyte cell line, EPC2-hTERT.

Project description:Eosinophilic esophagitis (EoE) is a chronic, allergic inflammatory disease of the esophageal mucosa. While type 2 cytokines are predominant, targeting type 2 inflammation alone is not always effective for all patients. In EoE patients, the transcriptional profiling of esophageal biopsy reveal upregulation of type I and II interferon (IFN) response, dysregulated immune signaling and downregulation of esophageal-specific genes in EoE patients. However, the role of interferon signaling during EoE is not fully understood. This study aims to investigate the impact of IFN signaling on esophageal epithelium and elucidate its role in EoE. IFN-γ stimulation of esophageal epithelial cells triggered disruption of tissue differentiation, epithelial barrier integrity and cytotoxicity, which are relevant features of EoE immunopathology. Beyond EoE, our findings offer insights into esophageal disorders which may involve increased IFN-γ signaling, including infections, gastrophageal reflux disease, and Barrett's esophagus.

2024-02-26 | GSE234424 | GEO