IC - Experiment 2
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE346 | GEO | 2003/07/14
SECONDARY ACCESSION(S): PRJNA84831
REPOSITORIES: GEO
Similar Datasets
Project description:Normal bladder epithelial cell explant from a single normal control was treated with APF from a single IC patient or mock APF. Two different membranes were used. Keywords: other
2003-07-14 | GSE345 | GEO
Project description:Changes in human bladder epithelial cell gene expression associated with interstitial cystitis or antiproliferative factor treatment. Explanted bladder epithelial cells from patients with interstitial cystitis (IC) have been shown to differ from explanted control cells in several ways, including production of an antiproliferative factor (APF), altered production of certain epithelial growth factors, and rate of proliferation. To better understand the role of the APF in abnormal bladder epithelial cell proliferation in IC, we studied gene expression patterns in normal bladder epithelial cells treated with APF vs. mock APF and compared them to expression patterns in IC vs. normal cells using microarray analysis. Oligo-dT-primed total cellular RNA was labeled with [33P]dCTP and hybridized to GeneFilter GF211 microarray membranes (Research Genetics) containing cDNA for 3,964 human genes. Thirteen genes that function in epithelial cell proliferation or differentiation were consistently differentially expressed in both IC (compared with control) and APF-treated (compared with mock APF-treated) normal bladder epithelial cells. The general pattern of gene expression in IC and APF-treated cells suggested a less proliferative phenotype, with increased expression of E-cadherin, phosphoribosylpyrophosphate synthetase-associated protein 39, and SWI/SNF complex 170-kDa subunit, and decreased expression of vimentin, {alpha}2-integrin, {alpha}1-catenin, cyclin D1, and jun N-terminal kinase 1; these findings were confirmed for the structural gene products (E-cadherin, vimentin, {alpha}2-integrin, and {alpha}-catenin) by immunohistochemistry. These results are compatible with the previously noted decreased proliferation rate of IC and APF-treated normal cells, and indicate that the mechanism whereby APF inhibits cell proliferation may involve both downregulation of genes that stimulate cell proliferation along with upregulation of genes that inhibit cell growth. Keywords: other
2003-09-03 | GSE621 | GEO
Project description:Changes in human bladder epithelial cell gene expression associated with interstitial cystitis or antiproliferative factor treatment. Explanted bladder epithelial cells from patients with interstitial cystitis (IC) have been shown to differ from explanted control cells in several ways, including production of an antiproliferative factor (APF), altered production of certain epithelial growth factors, and rate of proliferation. To better understand the role of the APF in abnormal bladder epithelial cell proliferation in IC, we studied gene expression patterns in normal bladder epithelial cells treated with APF vs. mock APF and compared them to expression patterns in IC vs. normal cells using microarray analysis. Oligo-dT-primed total cellular RNA was labeled with [33P]dCTP and hybridized to GeneFilter GF211 microarray membranes (Research Genetics) containing cDNA for 3,964 human genes. Thirteen genes that function in epithelial cell proliferation or differentiation were consistently differentially expressed in both IC (compared with control) and APF-treated (compared with mock APF-treated) normal bladder epithelial cells. The general pattern of gene expression in IC and APF-treated cells suggested a less proliferative phenotype, with increased expression of E-cadherin, phosphoribosylpyrophosphate synthetase-associated protein 39, and SWI/SNF complex 170-kDa subunit, and decreased expression of vimentin, {alpha}2-integrin, {alpha}1-catenin, cyclin D1, and jun N-terminal kinase 1; these findings were confirmed for the structural gene products (E-cadherin, vimentin, {alpha}2-integrin, and {alpha}-catenin) by immunohistochemistry. These results are compatible with the previously noted decreased proliferation rate of IC and APF-treated normal cells, and indicate that the mechanism whereby APF inhibits cell proliferation may involve both downregulation of genes that stimulate cell proliferation along with upregulation of genes that inhibit cell growth.
2010-06-05 | E-GEOD-621 | biostudies-arrayexpress
Project description:Cells from 6 different IC patients were run in parallel with cells from their 6 different matched controls. Keywords: other
2003-07-14 | GSE347 | GEO
Project description:Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic and debilitating pain disorder of the bladder and urinary tract with poorly understood etiology. A definitive diagnosis of IC/BPS can be challenging because many symptoms of IC/BPS are shared with other urological disorders. An analysis of urine presents an attractive and non-invasive resource for monitoring and diagnosing IC/BPS. Here, a non-targeted LC-MS and LC-MS/MS-based peptidomics analysis of urine samples collected from IC/BPS patients were compared to urine samples from asymptomatic controls.
2022-06-06 | PXD031843 | Pride
Project description:Notch1-IC, Notch2-IC or EBNA2 have been induced in a conditionally immortalized human B cell line (EREB2-5) in order to identify similar and unique target genes in B cells. CAT was used as a control. Experiment Overall Design: RNA was isolated at different time points after induction of Notch1-IC, Notch2-IC or EBNA2 in EREB2-5 cells. Three independent experiments were performed (except Notch1-IC at 3day).
2009-08-25 | E-GEOD-12355 | biostudies-arrayexpress
Project description:Interstitial cystitis/painful bladder syndrome (IC/PBS) is a chronic disease for which there is no effective treatment.Transforming Growth Factor-β (TGF-β) is thought to be involved in the pathogenesis of IC/PBS, and previous studies have shown that suggested that administration of TGF-β inhibitors significantly ameliorates IC/PBS in a mouse model.However, the molecular mechanism of the therapeutic effect of TGF-β inhibitors on IC/PBS has not been comprehensively analyzed. In this study, we show that TGF-β inhibitor administration ameliorated dysuria in IC/PBS mouse models using hydrogen peroxide through a variety of mechanisms.
2023-09-30 | GSE226802 | GEO
Project description:Interstitial cystitis (IC) is a progressive chronic bladder disease with an increasing incidence. Today, IC is diagnosed by subjective symptoms in combination with cystoscopic and histologic evidence. The ultimate goal is the development of a diagnostic assay for IC on a molecular level. A comparative gene expression profile of bladder biopsies from patients with IC and control patients identified candidate marker genes for IC. Experiment Overall Design: Five IC patients and six control patients ('healthy') have been selected for the study. All IC patients had Hunner's ulcers and, with the exception of one person, also glomerulations, whereas the control group did not show these cystoscopic findings. From each IC patient two biopsies have been taken, one from an ulcerated area of the bladder ('ulcus'), and one from an area that macroscopically looked 'normal', 'not-inflamed' or not hyperemic ('ni'). One 'ni' sample has been excluded from the study because it had an expression pattern similar to the healthy controls.
2009-05-14 | E-GEOD-11783 | biostudies-arrayexpress
Project description:Interstitial cystitis (IC) and bladder pain syndrome are terms used to describe a heterogenous chronic pelvic and bladder pain disorder of unknown etiology. The goal of this pilot study was to determine if gene expression profiling of bladder biopsy tissue from patients experiencing symptoms could be used to separate the patients based on some clinical parameter. Gene expression profiles in bladder biopsy tissue from patients with: (1) low bladder capacity (defined here as <400 ml upon hydordistension), (2) normal capacity (M-bM-^IM-%400 ml), and (3) controls were compared. Gene expression profiles from low bladder capacity tissues differed significantly from normal capacity and control tissue, suggesting gene expression profiling may be a useful tool for better understanding IC disease pathophysiology.
2014-05-13 | E-GEOD-57560 | biostudies-arrayexpress