Homo sapiens
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PROVIDER: PRJNA246701 | ENA |
REPOSITORIES: ENA
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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: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: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.
2014-05-13 | GSE57560 | 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:Gene expression analysis of urine sediment: evaluation for potential noninvasive markers of interstitial cystitis/bladder pain syndrome
| PRJNA139589 | ENA
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:Recent evidence suggests that the descending modulatory pathways from the brainstem rostral ventromedial medulla (RVM) are important for bladder inflammatory pain. This study aimed to identify the long-term molecular changes in RVM neurons due to early life cystitis during neuronal development and the effect of reexposure later in adulthood. RVM tissues from two treatment protocols were used: (1) neonatal zymosan exposures with acute adult rechallenge (RC) and (2) only neonatal zymosan exposures (NRC). RNAseq analysis showed upregulation of several genes associated with synaptic plasticity (Grin1, Grip2, Notch1, Arc, and Scn2b) in the cystitis groups compared to controls in both protocols. The RC protocol exhibited a stronger treatment effect with significantly higher fold differences between the groups compared to the NRC protocol (p<0.001, fold differences RC vs NRC). In microarrays, miR-34a-5p showed cystitis-induced downregulation in both protocols. Bioinformatics analysis identified multiple 3’UTRs complementary binding sites for miR-34a-5p on Grin2b, Notch1, Grip2, Scn2b, and Arc genes. The enhanced response in the RC protocol indicates a possible priming effect of early life cystitis on rechallenge in adulthood. These long-term molecular alterations may play a critical role in the development of chronic bladder pain conditions as seen in patients with Interstitial Cystitis/Bladder pain syndrome
2025-01-22 | GSE271334 | GEO
Project description:Gene expression profile of bladder tissue of patients with ulcerative interstitial cystitis
| PRJNA105977 | ENA
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: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