Correlation of gene expression with bladder capacity in interstitial cystitis/bladder pain syndrome
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE57560 | GEO | 2014/05/13
SECONDARY ACCESSION(S): PRJNA246701
REPOSITORIES: GEO
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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
Project description:Interstitial cystitis (IC)/bladder pain syndrome (BPS) is a clinical condition that manifests as a sensory hypersensitivity of unknown cause and is characterized by urinary frequency, bladder discomfort, and pelvic pain. In the present volatolomic study, we have analyzed the VOCs unique to urine specimens obtained from interstitial cystitis patients, in compassion to healthy controls.This is the novel finding from comprehensive and unbiased metabolomics analysis that urinary menthol is decreased in urine specimens from IC patients, and that the reduced menthol level in IC is potentially linked to the chronic inflammation, which is often observed in IC patients
2017-05-09 | ST000603 | MetabolomicsWorkbench
Project description:Interstitial cystitis (IC), a chronic bladder disease with an increasing incidence, is diagnosed using subjective symptoms in combination with cystoscopic and histological evidence. The ultimate goal is the development of a diagnostic assay for IC on a molecular level. By cystoscopic examination, IC can be classified into an ulcerative and a non-ulcerative subtype. To better understand this debilitating disease on a molecular level, a comparative gene expression profile of bladder biopsies from patients with ulcerative IC and control patients has been performed. Candidate marker genes for ulcerative IC were identified.
2009-05-01 | GSE11783 | 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:We compared the chnages in urinary bladder and iliac lymph nodes microRNAs in the control and experimental autoimmune cystitis in mice. A set of urinary bladder microRNAs (miRNAs) shows profound upregulation or downregulation in the expression profiles of the experimental IC as compared to control.
2021-06-12 | GSE177066 | 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:The pathogenesis of interstitial cystitis/bladder pain syndrome (IC/BPS) remains incompletely understood. Bladder fibrosis is a significant histopathological feature of IC/BPS, particularly in non-Hunner-type IC (NHIC). Transient receptor potential cation channel subfamily C member 3 (TRPC3) is known to play a crucial role in myocardial and renal fibrosis. This study investigates the involvement of TRPC3 in bladder fibrosis associated with IC/BPS. A rat model of IC/BPS was established using cyclophosphamide (CYP, 50 mg/kg, intraperitoneally, every 3 days for 3 doses). Bulk RNA sequencing was used to identify differentially expressed transient receptor potential (TRP) channel genes in CYP-induced cystitis rats, whereas single-cell RNA sequencing was utilized to pinpoint the cell type predominantly expressing transient receptor potential cation channel subfamily C member 3 (TRPC3) . TRPC3 inhibition was achieved through intraperitoneal injection of Pyrazole 3 (Pyr3, 0.1 mg/kg or 1 mg/kg). Suprapubic mechanical allodynia was assessed using up-down method with von Frey filaments and micturition frequency was assessed by cystometry. The expression of TRPC3 and components of the transforming growth factor beta (TGF-β)/Smad signaling pathway (TGF-β, p-Smad2, and p-Smad3) in the bladder was analyzed by Western blot. Bladder fibrosis was assessed through Masson’s staining and detection of fibrosis markers (Vimentin, Collagen I, and Collagen III) using Western blot. The RNA and protein expression of TRPC3 was up-regulated in CYP-induced cystitis rats. TRPC3 inhibition led to significant improvements in suprapubic mechanical allodynia and reduced micturition frequency in CYP-induced cystitis rats. Western blot analyses revealed that markers of bladder fibrosis (Vimentin, Collagen I, and Collagen III) were markedly upregulated in CYP-induced cystitis rats. Masson’s staining showed an increased area of collagen fibers. Additionally, inhibition of TRPC3 resulted in significant downregulation of the TGF-β/Smad signaling pathway (TGF-β, p-Smad2, and p-Smad3) in CYP-induced cystitis rats. TRPC3 activation contributes to bladder fibrosis in IC/BPS. Inhibition of TRPC3 ameliorates suprapubic mechanical allodynia and micturition frequency in CYP-induced cystitis rats by downregulating the TGF-β/Smad pathway. TRPC3 represents a potential therapeutic target for managing bladder fibrosis in IC/BPS.
2025-03-31 | GSE293339 | 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:We report the application of single cell RNA-seq for transcript profiling in bladder tissue from Interstitial cystitis/bladder pain syndrome (IC/BPS) with Hunner lesions and without Hunner lesions and normal tissue.
2024-05-23 | GSE175526 | GEO
Project description:Hunner-type interstitial cystitis (HIC) is a rare, enigmatic inflammatory disease of the urinary bladder with no curative treatments. In this study, we aimed to characterize the unique cellular and immunological factors specifically involved in HIC by comparing with cystitis induced by Mycobacterium bovis bacillus Calmette–Guérin, which presents similar clinicopathological features to HIC. Here, we show that T helper 1/17 polarized immune responses accompanied by prominent overexpression of interferon (IFN)-γ, enhanced cGAS-STING cytosolic DNA sensing pathway, and increased plasma cell infiltration are the characteristic inflammatory features in HIC bladder. Further, we developed a novel mouse anti-IFN-γ DNA aptamer and observed that intravesical instillation of the aptamer significantly ameliorated bladder inflammation, pelvic pain and voiding dysfunction in a recently developed novel murine HIC mouse model with little migration into the blood. Our study provides the plausible basis for clinical translation of the anti-IFN-γ DNA aptamer in the treatment of human HIC.
2023-07-29 | GSE238208 | GEO