Intestinal epithelial cell Caspase 8 ablation colitis and ileitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB78544 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR13431762_1.fastq.gz | Fastqsanger.gz | |||
| ERR13431762_2.fastq.gz | Fastqsanger.gz | |||
| ERR13431763_1.fastq.gz | Fastqsanger.gz | |||
| ERR13431763_2.fastq.gz | Fastqsanger.gz | |||
| ERR13431764_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:Part of a mouse inflammation model set in order to observe the similarities and differences between the multiple options for the generation of intestinal inflammation in an animal model. Experimental samples are generated according to the standard protocol for the model. and are processes using the same set of bioinformatic tools.
2025-01-30 | E-MTAB-14318 | biostudies-arrayexpress
Project description:Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8. We used microarrays to investigate the difference of the global programme of gene expression in intestinal epithelial cells of control and caspase-8 deficient mice. Intestinal epithelial cells were isolated from 3 control mice and 3 mice with a conditional deletion of caspase-8 in the intestinal epithelium. RNA was isolated and subjected to Affymetrix gene chip analysis.
2011-07-22 | E-GEOD-30873 | biostudies-arrayexpress
Project description:Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8. We used microarrays to investigate the difference of the global programme of gene expression in intestinal epithelial cells of control and caspase-8 deficient mice.
2011-07-23 | GSE30873 | GEO
Project description:In this study, we investigated regional and sex differences in the cholinergic modulation of intestinal epithelial cells in homeostasis and regeneration. Genetic intestinal epithelial ablation of the M3R employing Vil-Cre x M3R fl/fl mice interestingly resulted in the prominent reduction in Lgr5-expressing progenitor cells in male tissues, contrasting an expansion of these cells in the female intestinal epithelium. This prominent difference showed abrogated in young female mice with reduced circulating sex hormone levels. M3R ablation further induced the expansion of pEGFR+ tuft cells and induced the activation of the PI3K/Akt pathway. Importantly, sex-specific differences in Lgr5-expressing progenitor cells translated into the development of severe inflammation in male Vil-Cre x M3R fl/fl mice subjected to an acute colitis model, which did almost not affect female Vil-Cre x M3R fl/fl mice. In addition, sex-specific effects of modulations of cholinergic signaling on epithelial cells could be corroborated in murine and human colonoids. Collectively, our data reveal regional and sex differences in the cholinergic, muscarinic modulation of intestinal epithelial cells.
2025-02-28 | GSE286189 | GEO
Project description:In this study, we investigated regional and sex differences in the cholinergic modulation of intestinal epithelial cells in homeostasis and regeneration. Genetic intestinal epithelial ablation of the M3R employing Vil-Cre x M3R fl/fl mice interestingly resulted in the prominent reduction in Lgr5-expressing progenitor cells in male tissues, contrasting an expansion of these cells in the female intestinal epithelium. This prominent difference showed abrogated in young female mice with reduced circulating sex hormone levels. M3R ablation further induced the expansion of pEGFR+ tuft cells and induced the activation of the PI3K/Akt pathway. Importantly, sex-specific differences in Lgr5-expressing progenitor cells translated into the development of severe inflammation in male Vil-Cre x M3R fl/fl mice subjected to an acute colitis model, which did almost not affect female Vil-Cre x M3R fl/fl mice. In addition, sex-specific effects of modulations of cholinergic signaling on epithelial cells could be corroborated in murine and human colonoids. Collectively, our data reveal regional and sex differences in the cholinergic, muscarinic modulation of intestinal epithelial cells.
2025-02-28 | GSE286190 | GEO
Project description:In the present study, we demonstrated that mice deficient in chemerin or IEC-specific CMKLR1 expression were highly susceptible to DSS-induced colitis and subsequent tumorigenesis, which was reversed by suppressing colonic neutrophilic inflammation using CXCR2 inhibitor. Surprisingly, we found that lack of the Chemerin-CMKLR1 signaling specifically reduced colonic epithelial expression of lactoperoxidase (LPO), an epithelial peroxidase which could utilize H2O2 to oxidase thiocyanates to antibiotic compound (Bafort et al., 2014). Importantly, we demonstrated that impaired epithelial LPO expression accounted for outgrowth of potentially pathogenic Gram-negative bacteria following epithelial injury, which led to overproduction of CXCL1/2 and pathological neutrophilic inflammation in mice with epithelial Chemerin-CMKLR1 signaling deficiency. Finally, lack of epithelial Chemerin-CMKLR1 signaling impaired early host defense against enteric bacteria, which was reversed by LPO supplementation. Taken together, our study uncovers a critical role of epithelial Chemerin-CMKLR1 signaling in restricting pathological colonic neutrophilia via potentiating LPO-mediated epithelial innate defense, thereby rendering protection against microbiota-driven colitis and tumorigenesis.
2022-06-30 | GSE178308 | GEO
Project description:Purpose: The objective of this study is to compare the transcriptome profile of intestinal epithelial organoids cultivated from distal colon tissue of patients with ulcerative colitis vs organoids cultivate from non-matched and otherwise healthy patient colon
2018-07-15 | GSE102746 | GEO
Project description:Caspase 9-induced apoptosis for efficient fetal cell ablation and disease modeling
| PRJNA1187456 | ENA
Project description:Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from DSS-induced murine colitis. While tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal Disease Activity Index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation Total RNAs from the colon of three control and three Hdac2 IEC-specific knockout mice were isolated with the Rneasy kit (Qiagen, Mississauga, ON, Canada).
2014-02-08 | E-GEOD-54785 | biostudies-arrayexpress
Project description:Inflammatory caspases are essential effectors of inflammation and cell death. Here, we investigated their roles in colitis and colorectal cancer and report a bimodal regulation of intestinal homeostasis, inflammation and tumorigenesis by caspases-1 and -12. Casp1-/- mice exhibited defects in mucosal tissue repair and succumbed rapidly after dextran sulfate sodium (DSS) administration. This phenotype was rescued by administration of exogenous interleukin-18 and was partially reproduced in mice deficient in the inflammasome adaptor ASC. Casp12-/- mice, in which the inflammasome is derepressed, were resistant to acute colitis and showed signs of enhanced repair. Together with their increased inflammatory response, the enhanced repair response of Casp12-/- mice rendered them more susceptible to colorectal cancer induced by azoxymethane (AOM)+DSS. Taken together, our results indicate that the inflammatory caspases are critical in the induction of inflammation in the gut following injury, which is necessary for tissue repair and maintenance of immune tolerance. Total RNA obtained from isolated tumors or normal colon tissue from wild type and caspase-12 deficient mice were compared.
2010-07-30 | E-GEOD-20407 | biostudies-arrayexpress