Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379846 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Esophageal epithelium of WT mice Esophageal epithelium of Pax9 KO mice
| PRJNA379477 | ENA
Project description:Gene expression data from crypts isolated from WT and Lpcat3 Villin-CreERT2 mice
| PRJNA385328 | ENA
Project description:We aimed to determine the effects of p63KO and p63KO/Cdx2 overexpression on gene expression profiles in the mouse esophageal epithelium (P0).
2020-03-20 | GSE96831 | GEO
Project description:The ketogenic diet has been successful in promoting weight loss among patients that have struggled with weight gain. This is due to the cellular switch in metabolism that utilizes liver-derived ketone bodies for the primary energy source rather than glucose. Fatty acid transport protein 2 (FATP2) is highly expressed in liver, small intestine, and kidney where it functions in both the transport of exogenous long chain fatty acids (LCFA) and in the activation to CoA thioesters of very long chain fatty acids (VLCFA). We have completed a multi-omic study of FATP2-null (Fatp2-/-) mice maintained on a ketogenic diet (KD) or paired control diet (CD), with and without a 24-hour fast (KD-fasted and CD-fasted) to address the impact of deleting FATP2 under high-stress conditions. Control (wt/wt) and Fatp2-/- mice were maintained on their respective diets for 4-weeks. Afterwards, half the population was sacrificed while the remaining were fasted for 24-hours prior to sacrifice. We then performed paired-end RNA-sequencing on the whole liver tissue to investigate differential gene expression. The differentially expressed genes mapped to ontologies such as the metabolism of amino acids and derivatives, fatty acid metabolism, protein localization, and components of the immune system’s complement cascade, and were supported by the proteome and histological staining.
2020-06-10 | GSE152110 | GEO
Project description:Esophageal adenocarcinoma (EA) is increasingly common. EA is thought to arise from a precursor lesion, Barrett’s esophagus (BE), in which chronic bile and acid reflux from the stomach injures the esophagus and induces the esophageal squamous epithelium to transition to a mixed gastric and intestinal glandular mucosa. The molecular determinants driving this metaplasia are poorly understood. We established a biobank of human patient-derived BE organoids that recapitulated the molecular heterogeneity of BE. Bulk and single-cell transcriptomics, corroborated with analysis of patient tissues, pointed to BE differentiation depending on a balance between two transcription factors that govern foregut versus hindgut embryonic gastrointestinal development: SOX2 (driving esophageal and stomach differentiation) and CDX2 (driving intestinal differentiation). Using squamous-specific inducible Sox2 knockout (Krt5CreER/+; Sox2Δ/Δ;ROSA26LSLTdTomato/+) mice, we found increased basal proliferation and decreased differentiation in the foregut squamous epithelium. Remarkably, Sox2Δ/Δ mice also harbored expanded glands at the squamocolumnar junction, some of which lineage traced to Krt5-expressing cells, indicating metaplasia from squamous epithelium. CUT&RUN analysis showed SOX2 bound and promoted differentiation-associated (e.g.,Krt13) and repressed proliferation-associated (e.g., Mki67) targets. Thus, SOX2 is critical for foregut squamous epithelial differentiation and its decreased expression likely an initiating step in progression to BE and thence to EA.
2025-06-07 | PXD063992 | Pride
Project description:Cdx2 has been suggested to play an important role in Barrett's esophagus (BE), or intestinal metaplasia (IM) in the esophagus. However, in vivo data have been lacking. The aim of the present study was to investigate whether transgenic overexpression of zCdx1b, the functional equivalent of mammalian Cdx2 in zebrafish, may lead to IM of squamous epithelium in zebrafish A transgenic zebrafish system was developed by expressing zCdx1b gene under the control of zebrafish keratin 5 promoter (zK5p). zCdx1b expression in the esophageal squamous epithelium of transgenic zebrafish was analyzed by in situ hybridization, immunohistochemical staining and RT-PCR. Gene expression in the esophageal squamous epithelium of wild-type and transgenic zebrafish was analyzed by Affymetrix microarray and confirmed by in situ hybridization.
2012-02-18 | GSE35889 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.
2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress
Project description:Esophageal adenocarcinoma (EAC) has the fastest increase of any cancer in the US and Europe, and arises in the setting of BarrettM-bM-^@M-^Ys esophagus (BE), defined by replacement of normal squamous epithelium with columnar intestinal-like epithelium. BE is thought to result from chronic esophageal inflammation but has been elusive to model in animals. Herein, we have generated the first transgenic mouse model of BarrettM-bM-^@M-^Ys esophagus through overexpression of interleukin-1M-CM-^_ (IL-1M-NM-2). IL-1M-NM-2 overexpression in the mouse esophageal mucosa induces chronic inflammation that progresses to intestinal metaplasia, with characteristic expression of TFF2, Bmp4 and Cdx2. With aging, IL-1b transgenic mice progress to esophageal adenocarcinoma (EAC) but the process is markedly accelerated by exposure to bile acids and/or nitrosamines, resembling the human counterpart. Moreover, progenitor cells present in the gastric cardia, but absent from the esophagus in humans and mice, are increased in BE, suggesting the cell of origin in the gastric cardia Comparison of BE and EAC tissue from the mouse with normal squamous epithelium from the mouse.
2011-01-31 | E-GEOD-24931 | biostudies-arrayexpress
Project description:Cdx2 has been suggested to play an important role in Barrett's esophagus (BE), or intestinal metaplasia (IM) in the esophagus. However, in vivo data have been lacking. The aim of the present study was to investigate whether transgenic overexpression of zCdx1b, the functional equivalent of mammalian Cdx2 in zebrafish, may lead to IM of squamous epithelium in zebrafish A transgenic zebrafish system was developed by expressing zCdx1b gene under the control of zebrafish keratin 5 promoter (zK5p). zCdx1b expression in the esophageal squamous epithelium of transgenic zebrafish was analyzed by in situ hybridization, immunohistochemical staining and RT-PCR. Gene expression in the esophageal squamous epithelium of wild-type and transgenic zebrafish was analyzed by Affymetrix microarray and confirmed by in situ hybridization. The upper digestive tract tissue from 3 adult zebrafish (3 months old) was pooled as one sample. Three zCdx1b transgenic samples were used for microarray, and 2 wild type samples were used for control.
2012-02-18 | E-GEOD-35889 | biostudies-arrayexpress