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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE68276 | GEO | 2015/10/01

SECONDARY ACCESSION(S): PRJNA282371

REPOSITORIES: GEO

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Cell cloning of Barrett's esophagus stem cell, gastric cardia stem cells and normal esophagus stem cells

Project description:Barrett’s esophagus confers significant risk of esophageal adenocarcinoma. We have established the cloning of patient-matched stem cells of Barrett’s, gastric, and esophageal epithelium. Barrett's esophagus stem cells (BE), gastric cardia stem cells (GC) and normal esophagus stem cells (Eso) from 12 patients were cloned (For BE: 12 patients, GC: 12 patients and Eso: 2 patients). Keratin 5 positive and Keratin 7 positive cells were cloned from human fetal esophageal epithelium. Using air liquid interface culture system, stem cells were induced to differentiate into mature epithelial structures.

2015-10-01 | GSE65013 | 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

Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

Project description:iASPP (PPP1R13L) is an evolutionarily conserved regulator of p53 family members. In mice, iASPP deletion in keratin 14-expressing keratinocytes is sufficient to cause detrimental phenotypes with squamous epithelium abnormalities. In human skin, wild-type nuclear iASPP colocalizes with the key squamous differentiation regulatory factor, TP63, and iASPP mutations are associated with abnormalities in skin development. To clarify how iASPP modulates p63 genome occupancy, p63 ChIP-seq data from iASPP WT and iASPP KO primary mouse keratinocytes (MKC) were compared.

2022-10-25 | GSE188447 | GEO

Following the p63/Keratin5 Basal Cells in the Sensory and Nonsensory Epithelia of The Vomeronasal Organ

Project description:The Vomeronasal organ (VNO) is a part of the accessory olfactory system, which is responsible for detecting pheromones, chemical factors that trigger a spectrum of sexual and social behaviors. The vomeronasal epithelium (VNE) shares several features with the epithelium of the main olfactory epithelium (MOE). However, it is a distinct neuroepithelium populated by chemosensory neurons that differ from the olfactory sensory neurons (OSNs) in cellular structure, receptor expression, and connectivity. The vomeronasal organ of rodents comprises a sensory epithelium and a thin nonsensory epithelium that morphologically resembles the respiratory epithelium. Sox2-positive cells have been previously identified as the stem cell population that gives rise to neuronal progenitors in MOE and VNE. In addition to these, the MOE also comprises p63 positive horizontal basal cells (HBCs), a second pool of quiescent stem cells that become active in response to injury. Immunolabeling against the transcription factor p63, Keratin-5 (Krt5), Krt14 and Krt5Cre tracing experiments highlighted the existence of horizontal basal cells distributed along the basal lamina of the VNO forming from progenitors along the basal lamina oft the marginal zones. Moreover, these experiments revealed that the NSE of rodents is, like the respiratory epithelium, a stratified epithelium where the p63/Krt5+ basal cells self-replicate and give rise to the apical columnar cells facing the lumen of the VNO.

2024-03-11 | GSE247872 | GEO

Genome-wide transcription factor binding and histone mark profiling in pluripotent and lineage-committed cells

Project description:Purpose: Assess changes in p63 binding in human embryonic stem cells and surface ectoderm; evaluate differences in the following histone marks: H3K27me3, H3K27ac, H3K4me1, and H3K4me3 in the surface ectoderm with and without p63; and examine changes in H3K27me3 between human embyronic stem cells and surface ectoderm with and without p63. Methods: p63 ChIP-seq libraries were generated in p63 gain-of-function human embryonic stem cells and wild-type surface ectoderm. H3K27me3 ChIP-seq libraries were generated in wild-type and p63 gain-of-function human embryonic stem cells as well as wild-type and p63 knockout surface ectoderm. H3K27ac, H3K4me1, and H3K4me3 ChIP-seq libraries were generated in wild-type and p63 knockout surface ectoderm. All ChIP-seq experiments were performed in duplicate and sequenced on Illumina NextSeq 500 sequencer. To ensure quality reads, fastq files were analyzed using FASTQC. Bowtie was used for read mapping and the parameters were as follows: -p 24 -S -a -m 1 --best --strata. For peak calling using MACS2, default settings were specified with a p-value of 0.05. To ensure quality peaks, IDR was run on all files, specifying FDR of 1% or 5% (or 10% for some broadPeak histone marks). Results: Limited changes in p63 binding in human embryonic stem cells and surface ectoderm; global loss of H3K37me3 without p63 in the surface ectoderm; limited differences in H3K27ac, H3K4me1, and H3K4me3 +/- p63 in the surface ectoderm; and increase in H3K27me3 with ectopic expression of p63 in human embryonic stem cells. Conclusion: p63 is able to bind it's surface ectoderm target sites regardless of the epigenetic landscape; p63 promotes H3K27me3 accumulation; and p63 does not regulate histone marks H3K27ac, H3K4me1, or H3K4me3

2018-11-06 | GSE122128 | GEO

FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

Project description:This study was designed to examine the requirement for the p63 transcription factor in Squamous Cell Carcinoma (SCC) tumor maintenance in an in vivo murine system. A tamoxifen-inducible Keratin 14-driven Cre recombinase transgene was used to conditionally excise p63 in advanced murine SCC tumors. These data show the context-dependent regulation of p63 target genes in cancer. Total RNA from murine Squamous Cell Carcinoma tumors was examined 1-3 days following genomic excision of TP63 in Keratin 14-expressing tumor cells.

2013-08-06 | E-GEOD-45929 | biostudies-arrayexpress

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Project description:Lung injury activates potential stem cells or progenitors for alveolar repair and regeneration. However, the activation program and source of injury-induced facultative progenitors remain incompletely known. Here, we find that lung injury induces emergence of p63-expressing progenitors, which rapidly proliferate and differentiate into alveolar type-1 (AT1) and type-2 (AT2) cells. scRNA-seq analysis uncovers that a subset of p63+ progenitors exhibit two distinct parallele transient stages before differentiation into mature AT1 and AT2 cells, respectively. Dual recombinases-mediated sequential genetic tracing reveals that facultative p63+ progenitors originate from the distal airway secretory cells and subsequently regenerate alveoli. Functioanlly, secretory cell-specific knockout of p63 significantly impairs their contribution to alveolar epithelium during lung regeneration. Our study identified secretory cell-derived facultative p63+ progenitors that contribute to alveolar regeneration, indicating a potential therapeutic target for lung treatment after injuires.

2023-02-20 | GSE225187 | GEO

Mus musculus

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

| PRJNA282371 | ENA

FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

2013-08-06 | GSE45929 | GEO

Whole transcriptome bisufilte sequencing for multiple species [NSUN2 verification]

Project description:(1) We cloned and transfected human xenogenic (zebrafish, mouse, etc.) NSUN2 into human NSUN2 knockout cells.(2) We treated wild-type human cells with nocodazole.

2022-02-27 | GSE160594 | GEO

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