Mus musculus
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ABSTRACT:
PROVIDER: PRJNA163077 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome analysis of mRNAs extracted from the rectal mucosa of WT and α6ΔIEC-TAM mice, 15 days after tamoxifen treatment Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. We show that the specific ablation of integrin α6 in intestinal epithelial cells (IECs) results in spontaneous colorectal inflammation in mice. In order to characterize the earlier molecular signature involved in the onset of inflammation, we performed Affymetrix microarrays and compare control versus α6ΔIEC-TAM transcriptomes after tamoxifen treatment.
2016-07-07 | GSE70700 | GEO
Project description:Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. It has been largely documented that IBD frequently lead to colorectal cancers (CRC). The identification of causative factors of IBD is thus essential to understand CRC progression and develop therapeutical approaches. Models have been described in which molecular alterations are combined with inflammatory treatments in order to recapitulate IBD-associated CRC. Here, we describe a mouse line, α6fl/fl Villin-Cre, in which inactivation of the gene encoding the integrin alpha-6 subunit (ITGA6) specifically in the intestinal mucosa results into chronic inflammation and intestinal carcinogenesis. In these mice, the loss of integrin alpha-6 beta-4, a receptor mediating the attachment of epithelial cells to laminins, leads to epithelial detachment, hyperplasia, chronic inflammation, rectal prolapses, and ultimately adenocarcinomas. Alterations of differentiation affecting mucus secreting (goblet) cells as well as changes in expression of essential intestinal transcription factors were detected. Thus alpha-6 beta-4 integrin is a key factor for the maintenance of intestinal integrity and its loss may represent a risk factor for tumor progression associated with IBD. Transcriptome analysis of RNA from normal versus inflamed and carcinomatous rectal mucosa of α6 integrin deficient intestinal epithelium mice was performed. RNAs were prepared from 5 adenocarcinomas, which were macrodissected from the rectal prolapses and 4 flanking inflamed rectal mucosa of 53-80 week-old α6fl/fl Villin-Cre mice. RNAs from normal rectal mucosa were obtained by rectum scraping from 4 matched control animals. The transcriptome analysis was performed using the Affymetrix Mouse Gene 1.0 ST arrays. Images were processed using affymetrix GeneChip® Command Console® Software (AGCC) (version 2.0) and numerical value were generated using Affymetrix Expression Console⢠Software (version 1.1).
2016-07-07 | E-GEOD-37749 | biostudies-arrayexpress
Project description:Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. It has been largely documented that IBD frequently lead to colorectal cancers (CRC). The identification of causative factors of IBD is thus essential to understand CRC progression and develop therapeutical approaches. Models have been described in which molecular alterations are combined with inflammatory treatments in order to recapitulate IBD-associated CRC. Here, we describe a mouse line, α6fl/fl Villin-Cre, in which inactivation of the gene encoding the integrin alpha-6 subunit (ITGA6) specifically in the intestinal mucosa results into chronic inflammation and intestinal carcinogenesis. In these mice, the loss of integrin alpha-6 beta-4, a receptor mediating the attachment of epithelial cells to laminins, leads to epithelial detachment, hyperplasia, chronic inflammation, rectal prolapses, and ultimately adenocarcinomas. Alterations of differentiation affecting mucus secreting (goblet) cells as well as changes in expression of essential intestinal transcription factors were detected. Thus alpha-6 beta-4 integrin is a key factor for the maintenance of intestinal integrity and its loss may represent a risk factor for tumor progression associated with IBD.
2016-07-07 | GSE37749 | GEO
Project description:Transcriptome analysis of mRNAs extracted from the rectal mucosa of WT and α6ÎIEC-TAM mice, 15 days after tamoxifen treatment Inflammatory bowel diseases (IBD) in humans are characterized by chronic inflammation and gastrointestinal tissue damage, caused by a combination of genetic and environmental factors. We show that the specific ablation of integrin α6 in intestinal epithelial cells (IECs) results in spontaneous colorectal inflammation in mice. In order to characterize the earlier molecular signature involved in the onset of inflammation, we performed Affymetrix microarrays and compare control versus α6ÎIEC-TAM transcriptomes after tamoxifen treatment. RNAs were prepared from rectal mucosa of 3 control mice treated with tamoxifen, 4 mutant mice treated with tamoxifen and 4 mutant mice treated with NaCl. The transcriptome analysis was performed using the Affymetrix Mouse Gene 1.0 ST arrays. Images were processed using affymetrix GeneChip® Command Console® Software (AGCC) (version 2.0) and numerical values were generated using Affymetrix Expression Console⢠Software (version 1.1).
2016-07-07 | E-GEOD-70700 | biostudies-arrayexpress
Project description:Transcriptional profile of murine touch dome keratinocytes sorted on the basis of alpha6-integrin, CD34, Sca1 and CD200 surface markers. Compared to the transcriptional profile of murine interfollicular epidermis (IFE) without the touch dome keratinocytes
2010-11-15 | E-MEXP-2925 | biostudies-arrayexpress
Project description:Spontaneous pancreatitis caused by tissue-specific gene ablation of Hhex in mice
| PRJNA268145 | ENA
Project description:Integrin alpha 6 (ITGA6) forms integrin receptors with either integrin β1 (ITGB1) or integrin beta 4 (ITGB4). To study its expression and regulatory functions in hepatocellular carcinoma (HCC) progression, whole transcriptome RNA sequencing in paired HCC tumor and adjacent non-tumor liver tissue samples from ten local Hispanic patients was performed. The average expression of ITGA6 was found increased by over 3.5-fold in HCC tumor tissues in comparison with their adjacent non-tumor tissues. The study indicates integrin alpha6-beta4 complex as a potential therapeutic target for treating patients in HCC.
2022-05-18 | GSE202853 | GEO
Project description:We performed RNA-seq on purified squamous cell carcinoma stem cells (SCC-SCs) from primary mouse skin tumors transduced with TGF-beta reporter. SCC-SCs were purified based on cell surface marker expression integrin alpha6 and CD44, after lineage negative selection, and separated by fluorescent TGF-beta reporter expression.
2015-02-27 | E-GEOD-64867 | biostudies-arrayexpress
Project description:Hepatic cirrhosis or advanced fibrosis caused by chronic hepatitis may be the main risk factor contributing to the occurrence of HCC. Growing clinical evidence show that patients with hepatic cirrhosis or advanced fibrosis may have a 7-fold higher incidence rate of HCC than those without, suggesting a crucial role of inflammation-carcinogenesis malignant transformation in HCC development and progression. We used microarrays to detail the global programme of gene expression underlying inflammation-carcinogenesis malignant transformation in HCC and identified distinct classes of up-regulated and down-regulated genes during this process
2021-02-12 | GSE166163 | GEO
Project description:Innate lymphoid cells (ILCs) are critically involved in intestinal adaptation to microenvironmental challenges (Colonna, 2018; Guendel et al., 2020) and the gut mucosa is characterized by low oxygen. Adaptation to low oxygen is mediated by Hypoxia-inducible transcription factors (HIFs) the HIF-1α subunit shapes the ILC phenotype upon acute experimental colitis and contributes to intestinal damage. However, the impact of HIF signaling in NKp46+ ILC in the context of repetitive mucosal damage and chronic inflammation, as it typically occurs during inflammatory bowel disease, is unknown. In a model of chronic colitis, mice lacking the HIF-1α isoform in NKp46+ ILCs show a decrease in NKp46+ ILC1s but a concomitant rise in neutrophils as well as Ly6C high macrophages. Single-nuclei RNA sequencing suggests enhanced interaction of mesenchymal cells with other cell compartments in the colon of HIF-1α KO mice and a loss of mucus-producing enterocytes as well as intestinal stem cells. This was, furthermore, associated with increased BMP-integrin signaling, expansion of profibrotic fibroblasts subsets and intestinal fibrosis. In summary this suggests that HIF-1 α mediated ILC1 activation, although detrimental upon acute colitis, protects against excessive inflammation and fibrosis during chronic intestinal damage.
2024-06-12 | GSE252602 | GEO