Human bladder cell spatial mapping
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE297459 | GEO | 2025/12/19
REPOSITORIES: GEO
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Project description:Human PBMC RNA Expression, Nanostring custom probe panel
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Project description:Objectives: Much of the information to date in terms of subtypes and function of bladder urothelial cells were derived from anatomical location or by the expression of a small number of marker genes. To have a comprehensive map of the cellular anatomy of bladder urothelial cells, we performed single-cell RNA-sequencing to thoroughly characterize mouse bladder urothelium. Materials and methods: A total of 18,917 single cells from mouse bladder urothelium was analyzed by unbiased single-cell RNA sequencing. The expression of the novel cell marker was confirmed by immunofluorescence using urinary tract infections models. Results: Unsupervised clustering analysis identified 8 transcriptionally distinct cell subpopulations from mouse bladder urothelial cells. We discovered a novel type of bladder urothelial cells marked by Plxna4 that may be involved with host response and wound healing. We also found a group of basal-like cells labeled by ASPM that could be the progenitor cells of adult bladder urothelium. ASPM+ urothelial cells are significantly increased after injury by UPEC. In addition, specific transcription factors were found to be associated with urothelial cell differentiation. At the last, a number of interstitial cystitis/bladder pain syndrome-regulating genes were found differentially expressed among different urothelial cell subpopulations. Conclusions: Our study provides a comprehensive characterization of bladder urothelial cells, which is fundamental to understanding the biology of bladder urothelium and associated bladder disease.
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Project description:Fifty patient urine samples diagnosed as high-grade urothelial carcinoma (HGUC) or benign were evaluated for bladder cancer via urine cytology. RNA was isolated and analyzed by microarray to identify a panel of biomarkers differentially expressed in HGUC and benign.
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Project description:Aneuploidy is among the most common hallmarks of cancer, yet the underlying genetic mechanisms are still poorly defined. We have recently identified STAG2 as a gene that is mutated in human cancer and whose inactivation leads directly to chromosomal instability and aneuploidy. However, no single tumor type has yet been identified in which inactivation of a cohesin subunit represents a predominant mutational event. Here we used immunohistochemistry to screen a panel of 2,214 tumors from each of the major human tumor types to identify additional tumor types harboring somatic loss of STAG2. Strikingly, STAG2 expression was completely absent in 18% of urothelial carcinomas, the most common type of bladder cancer and the fifth most common cancer in the United States. DNA sequencing revealed that somatic mutations of STAG2 were present in 21% of urothelial carcinomas, which were found to be a group of highly aneuploid tumors. The acquisition of STAG2 mutations was shown to be an early event in the pathogenesis of urothelial carcinoma. STAG2 loss was significantly associated with lymph node invasion, increased disease recurrence, and reduced cancer-specific survival. These results identify STAG2 as one of the most commonly mutated genes in bladder cancer discovered to date, and demonstrate that STAG2 inactivation defines an aggressive subtype of bladder cancer with particularly poor prognosis. Affymetrix CytoScan HD Arrays were performed according to the manufacturer's directions on genomic DNA extracted directly from snap-frozen human urothelial carcinoma primary tumors. Copy number analysis using Affymetrix CytoScan HD Arrays was performed for 12 human urothelial carcinomas of the bladder with truncating mutations of the STAG2 gene.
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Project description:Host responses to intracellular UPEC communities; We used laser capture microdissection and microarrays to identify urothelial transcripts differentially expressed in response to proximity to intracellular UPEC. Experiment Overall Design: Transcription within four distinct populations of urothelial cells was profiled in biological duplicate: (i) uninfected, (ii) mock-infected (sterile 1x PBS), (iii) IBC-distal (cells residing >10 cell diameters from IBCs in the section plane), and (iv) IBC-proximal (cells residing <10 cell diameters from IBCs in the section plane).
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Project description:The Notch signaling pathway mediates cell-cell communication regulating cell differentiation and proliferation and cell fate decisions in various tissues. In the urinary bladder, Notch acts as a tumor suppressor in mice, while mutations in Notch pathway components have been identified in human bladder cancer as well. Here we report that the genetic inactivation of Notch in mice leads to downregulation of cell-cell and cell-ECM interaction components, including proteins previously implicated in interstitial cystitis/bladder pain syndrome (IC/BPS), structural defects and mucosal sloughing, inflammation, and leaky urine-blood barrier. Molecular profiling of ailing mouse bladders showed similarities with IC/BPS patient tissue, which also presented low Notch pathway activity as indicated by reduced expression of canonical Notch targets. Urothelial integrity was reconstituted upon exogenous reactivation of the Notch pathway, implying a direct involvement of Notch. Despite damage and inflammation, urothelial cells failed to proliferate, uncovering a possible role for α4 integrin in urothelial homeostasis. Our data uncover a broad role for Notch in bladder homeostasis involving urothelial cell crosstalk with the microenvironment.
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Project description:<p>Hunner-type interstitial cystitis/bladder pain syndrome (HIC) is a complex and clinically challenging chronic disorder characterized by bladder-centered symptoms, including persistent pelvic pain and urinary urgency frequency, with elusive pathogenesis involving poorly defined multi-system interactions and systemic implications. To investigate upstream drivers of urothelial injury, we employed an integrative multi-omics approach, incorporating metagenomic sequencing, targeted metabolomics of urine and serum, and single-cell RNA sequencing. Our analysis identified Enterococcus avium, Megasphaera micronuciformis, and Fusobacterium nucleatum as the significantly enriched species in HIC patients, with bile acid metabolism appearing as a prominently altered pathway. Metabolomic profiling revealed the elevated levels of taurochenodeoxycholic acid (TCDCA) and tauroursodeoxycholic acid, while single-cell transcriptomic data pointed to TLR3 signaling as a key mediator of urothelial injury. Cross-omics correlation proposed a mechanistic axis involving E. avium, TCDCA, and TLR3 activation. Functional validation using fecal microbiota transplantation, E. avium transplantation, and TCDCA administration demonstrated that this axis contributes to the urothelial barrier disruption and inflammatory responses via TLR3. Intervention with a TLR3 inhibitor demonstrated therapeutic potential. These findings shed light on the pathogenesis of HIC, highlighting the potential role of the gut-bladder axis in disease development. This may contribute not only to the discovery of novel biomarkers but also to the development of personalized treatment strategies targeting specific molecular and microbial pathways.</p>
2025-12-16 | MTBLS13513 | MetaboLights