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Gene expression profiles of p63 knockout mouse

ABSTRACT: p63 is essential for the self-renewal of stem cells of all stratified epithelial tissues, including mammary and prostate glands as well as all squamous epithelia. In p63 null embryos, stratified epithelial tissues are lost or eroded several days after stratification due to the loss of regenerative cell populations. Here we show that p63 null embryos rapidly develop intestine-like metaplasia with gene expression profiles similar to Barrett’s metaplasia in a proximal stomach region. Also, we found that deletion of p63 cells in bladder leads to an expansion of columnar epithelial cells along the basement membrane and their rapid transition to a metaplastic phenotype similar to Barrett’s esophagus. It is likely that bladder carcinogens recapitulate this entire metaplastic transition.

ORGANISM(S): Mus musculus

PROVIDER: GSE65896 | GEO | 2024/06/30

REPOSITORIES: GEO

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Project description:Barrett's esophagus is characterized by the replacement of squamous epithelium with specialized intestinal metaplastic mucosa. The exact mechanisms of initiation and development of Barrett's metaplasia remain unknown, but a hypothesis of successful adaptation against noxious reflux components has been proposed. To search for the repertoire of adaptation mechanisms of Barrett's metaplasia, we employed high-throughput functional genomic and proteomic methods that defined the molecular background of metaplastic mucosa resistance to reflux. Transcriptional profiling was established for 23 pairs of esophageal squamous epithelium and Barrett's metaplasia tissue samples using Affymetrix U133A 2.0 GeneChips and validated by quantitative real-time polymerase chain reaction. Differences in protein composition were assessed by electrophoretic and mass-spectrometry-based methods. Among 2,822 genes differentially expressed between Barrett's metaplasia and squamous epithelium, we observed significantly overexpressed metaplastic mucosa genes that encode cytokines and growth factors, constituents of extracellular matrix, basement membrane and tight junctions, and proteins involved in prostaglandin and phosphoinositol metabolism, nitric oxide production, and bioenergetics. Their expression likely reflects defense and repair responses of metaplastic mucosa, whereas overexpression of genes encoding heat shock proteins and several protein kinases in squamous epithelium may reflect lower resistance of normal esophageal epithelium than Barrett's metaplasia to reflux components. Despite the methodological and interpretative difficulties in data analyses discussed in this paper, our studies confirm that Barrett's metaplasia may be regarded as a specific microevolution allowing for accumulation of mucosal morphological and physiological changes that better protect against reflux injury. Department of Gastroenterology, Medical Center for Postgraduate Education and Maria SkM-EM-^Bodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland 2 types of tissue sample derived from the same patient: > Normal squamous epithelium (NE) from patients with longsegment of BarretM-bM-^@M-^Ys epithelium > Metaplastic epithelium from BarrettM-bM-^@M-^Ys esophagus (BE)

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Gene expression profiles of p63 knockout mouse

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