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Keratin 5 Basal Cells are Temporally Regulated Developmental and Tissue Repair Progenitors in Bladder Urothelium.

ABSTRACT: Keratin 5 Basal Cells are Temporally Regulated Developmental and Tissue Repair Progenitors in Bladder Urothelium.

PROVIDER: PRJNA1044080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26919386_1.fastq.gz	Fastqsanger.gz
	SRR26919386_2.fastq.gz	Fastqsanger.gz
	SRR26919387_1.fastq.gz	Fastqsanger.gz
	SRR26919387_2.fastq.gz	Fastqsanger.gz
	SRR26919388_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Keratin 5 Basal Cells are Temporally Regulated Developmental and Tissue Repair Progenitors in Bladder Urothelium.

Project description:Urothelium forms a distensible yet impermeable barrier, senses and transduces stimuli, and defends the urinary tract from mechanical, chemical and bacterial injuries. Biochemical and genetic labeling studies support the existence of one or more progenitor populations with the capacity to rapidly regenerate the urothelium following injury, but slow turnover, a low mitotic index, and inconsistent methodologies obscure progenitor identity. The progenitor properties of basal Keratin 5 urothelial cells (K5-UC) have been previously investigated, but those studies focused on embryonic or adult bladder urothelium. Urothelium undergoes desquamation and apoptosis after birth, which requires postnatal proliferation and restoration. Therefore, we mapped the fate of bladder K5-UCs across postnatal development/maturation and following administration of cyclophosphamide to measure homeostatic and reparative progenitor capacities, respectively. In vivo studies demonstrate that basal K5-UCs are age-restricted progenitors in neonates and juveniles, but not in adult mice. Neonatal K5-UCs retain a superior progenitor capacity in vitro, forming larger and more differentiated urothelial organoids than adult K5-UCs. Accordingly, K5-UC transcriptomes are temporally distinct, with enrichment of transcripts associated with cell proliferation and differentiation in neonates. Induction of urothelial proliferation is sufficient to restore adult K5-UC progenitor capacity. Our findings advance the understanding of urothelial progenitors and support a linear model of urothelial formation and regeneration, which may have significant impact on therapeutic development or tissue engineering strategies.

2024-01-03 | GSE248463 | GEO

Single cell transcriptomes of mouse bladder urothelium uncover novel cell type markers and urothelial differentiation characteristics.

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.

2020-12-12 | GSE163029 | GEO

In vivo replacement of damaged bladder urothelium by Wolffian duct epithelial cells

Project description:The bladder’s remarkable regenerative capacity in response to injury had been thought to reside exclusively in its basal and intermediate cells. While examining consequences of DNA methyltransferase 1 (Dnmt1) inactivation in mouse embryonic bladder epithelium, we made the surprising discovery that Wolffian duct epithelial cells also support bladder regeneration. Conditional inactivation of Dnmt1 in mouse urethral and bladder epithelium triggered widespread apoptosis, depleted basal and intermediate bladder cells and disrupted Uroplakin protein expression. These events coincided with recruitment of Wolffian duct epithelial cells into Dnmt1 mutant urethra and bladder where they were reprogrammed to express bladder markers including FOXA1, Keratin 5, P63 and Uroplakin. This is the first evidence that Wolffian duct epithelial cells can be summoned in vivo to replace damaged bladder epithelium and function as a cell reservoir for bladder regeneration.

2018-07-19 | GSE115477 | GEO

Cell culture of p63 knock out and wild type bladder epithelial stem cell

Project description:Although there are several reports describing a stem cell fraction to form urothelium and lineage tracing studies in urinary bladder, it is still unclear about stem cells in mouse bladder epithelium. Here, we have established the cloning system of mouse stem cells from wild type and p63 knockout bladder. We isolated stem/progenitor cells from wild type and p63 knockout epithelium. From wild type bladder, we have cloned keratin 5-positive stem cells, and from p63 knockout epithelium, which loses basal cell fraction, we have cloned morphologically-distinct keratin 8 and claudin 3 positive stem cells, which may be reminiscent of intestinal metaplasia in bladder.

2015-10-01 | GSE68276 | GEO

Gene expression data of iPS clones before bladder urothelium differentiation

Project description:We developed a method for the directed differentiation of hiPSCs into mature stratified bladder urothelium.

2019-07-30 | GSE131371 | GEO

Rat-bladder-OAB - Proteomic analysis of urothelium of rats with detrusor overactivity induced by bladder outlet obstruction

Project description:Overactive bladder (OAB) syndrome is a condition that has four symptoms: urgency, urinary frequency, nocturia, and urge incontinence and negatively affects a patient’s life. Recently, it is considered that the urinary bladder urothelium is closely linked to pathogenesis of OAB. However, the mechanisms of pathogenesis of OAB at the molecular level remain poorly understood, mainly as a result of lack of modern molecular analysis. The goal of this study is to identify a potential target protein that could act as a predictive factor for effective diagnosis and aid in the development of therapeutic strategies for the treatment of OAB syndrome. We produced OAB in a rat model and performed the first proteomic analysis on the mucosal layer (urothelium) of the bladders of normal and OAB rats.

2018-02-09 | PXD007571 | Pride

RNA-SEQ analysis of the superficial, intermediate and basal cell layers of the bladder urothelium 24h after infection with UTI89 strain of E.coli and their adult female non-UTI controls.

Project description:Dissection and FACS cell sorting techniques were used to isolate the superficial, intermediate and basal cell types from the bladder urothelium of adult female mice following UTI infections, and their controls. This analysis will determine the transcriptional profile of each cell type, identify compartment specific transcripts, compartment specific transcript isoforms and cell-type specific noncoding RNAs.

2017-09-30 | GSE85491 | GEO

Loss of LPAR6 and CAB39L Dysregulate Basal to Luminal Urothelial Differentiation Program Contributing to Bladder Carcinogenesis

Project description:In vitro and in vivo studies including single cell sequencing showed that LPAR6 and CAB39L play a major role in regulating basal to luminal urothelial differentiation. Their loss of function contributed to bladder carcinogenesis by dysregulating urothelial differentiation program and sensitizing the urothelium to N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) induced cancers, which recapitulated luminal and basal subtypes of human bladder cancer.

2024-06-19 | GSE235455 | GEO

Gene expression data of iPS clones before bladder urothelium differentiation

Project description:Gene expression data of iPS clones before bladder urothelium differentiation

| PRJNA543410 | ENA

Transcription profiling of mouse detrusor, stroma and urothelium from neonatal bladder. (GUDMAP Series_id: 20)

Project description:The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing bladder. The central thesis is straightforward. The combination of microdissected and laser capture microdissection (LCM) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing urogenital system. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone. The data submitted here represents the gene expression profiles of compartmental bladder tissues collected through laser capture microscopy. Experiment Overall Design: Bladders were isolated from newborn SMGA/EGFP transgenic mice, embedded in OCT, frozen and sectioned (8 microns). Detrusor, stroma and urothelium were isloated using laser capture microscopy. The caps were frozen on dry ice and stored at -80 degrees C until RNA was extracted for gene expression analysis. Laser captured and total RNA isolated for gene expression analysis using the Affymetrix MOE430 microarray chip.

2008-06-11 | E-GEOD-11221 | biostudies-arrayexpress

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