Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA152515 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Age-dependent gene expression in isolated small intestinal epithelial cells (IECs)
| PRJNA152513 | ENA
Project description:A striking example of the intricate interplay between diet, microbiota, and host is the effect of inulin, a dietary fiber, on the intestinal epithelium. Ingestion of inulin triggers a wide range of epithelial effects in the colon, such as enhanced proliferation, increased production of mucus and antimicrobial peptides, as well as systemic effects on host metabolism and immune function that are dependent on microbiota-derived molecules. In this study, we investigated the impact of inulin on two critical aspects of diet-microbiota-host interactions: intestinal hypoxia and the modulation of hypoxia-inducible factor (HIF)-1 signaling in intestinal epithelial cells (IECs) in mice colon. To achieve this, we employed a multilayered and multi-omics approach, including dietary interventions, in vitro analysis using intestinal organoids, and both genetic and pharmacological interventions. We found that inulin intake enhances intestinal hypoxia, resulting in the stabilization of HIF-1 in IECs, an effect that is both microbiota- and host-dependent. Our study revealed that HIF-1 plays a key role in regulating IEC proliferation and intestinal stem cell (ISC) function. These changes are associated with HIF-1-dependent metabolic alterations in IECs. Our findings uncover a novel mechanism by which HIF-1 acts in the colon: it acts as a molecular brake, modulating cell proliferation in a microbiota-dependent manner and through metabolic reprogramming, highlighting the complexity of the diet-microbiota-host interactions in the gut.
2025-08-22 | PXD059757 | Pride
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs. mRNA and accessible chromatin (DNase-seq) profiles from colonic and ileal IECs were compared between conventionally-raised (CR), germ-free (GF), and conventionalized (CV) C57BL/6 mice.
2014-06-07 | E-GEOD-57919 | biostudies-arrayexpress
Project description:Transcriptional response of small intestinal epithelial cells (S-IECs) to bacterial monocolonization
| PRJNA345541 | ENA
Project description:Expression data from intestinal epithelial cells (IECs) [Mouse430_2 array]
| PRJNA247395 | ENA
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs.
2014-06-07 | GSE57919 | GEO
Project description:Remodeling of the gut microbiota is implicated in various metabolic and inflammatory diseases of the gastrointestinal tract. We hypothesized that the gut microbiota affects the DNA methylation profile of intestinal epithelial cells (IECs) which could, in turn, alter intestinal function. Here, we used mass spectrometry and methylated DNA capture to respectively investigate global and genome-wide DNA methylation of intestinal epithelial cells from germ-free (GF) and conventionally raised mice (CONV-R). In colonic IECs from GF mice, DNA was markedly hypermethylated. This was associated with a dramatic loss of Ten-Eleven-Translocation activity, a lower DNA methyltransferase activity and lower circulating levels of the one carbon metabolites cobalamin and folate. At the gene level, we found an enrichment for differentially methylated regions at proximity of genes regulating cytotoxicity of Natural Killer cells (FDR < 8.9E-6), notably members of the natural killer group 2 member D ligand superfamily Raet. Our results suggest that altered activity of methylation-modifying enzymes in GF mice influences the IEC epigenome at genes involved in the crosstalk between intestinal and immune cells. Epigenetic reprogramming of IECs by the gut microbiota may modulate intestinal function in diseases associated with altered gut microbiota.
2019-01-23 | GSE117434 | GEO
Project description:The intestinal epithelium plays a critical role in immune–microbiota interactions, yet its contribution to systemic autoimmunity remains unclear. Here, we identify intestinal epithelial cells (IECs) as key initiators of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). In MS patients, IECs upregulate antigen presentation–related genes and associate with increased intestinal Th17 cell accumulation.
2026-02-24 | GSE315728 | GEO
Project description:Expression data from intestinal epithelial cells (IECs) [MoGene-1_0-st array]
| PRJNA247394 | ENA
Project description:Mitochondrial stress triggers both metabolic and transcriptomic reprogramming but its effects on tumor development remains unclear. It is also unknown whether the genetic status has any influence on the capacity of mitochondrial stress to control tumor development. To explore these issues, we generated a mouse model lacking the lipid transfer protein Stard7 in intestinal epithelial cells (IECs) and assessed tumor development in both Wnt-dependent tumor initiation and in inflammation-driven tumor development. The loss of Stard7 in both models of intestinal tumors impaired mitochondrial Complex I activity, led to a severe metabolic and lipidomic reprogramming and potentiated mTORC1 activation. As a result, levels of enzymes involved in serine biosynthesis were enhanced in Stard7-deficient IECs showing or not constitutive Wnt signaling. Strikingly, despite similar molecular signatures upon Stard7 deficiency in intestinal crypts showing or not constitutive Wnt signaling, Stard7 contributed to tumor development in AOM/DSS-treated mice but inhibits Wnt-driven cancer initiation in the intestine. Apc+/min mice lacking Stard7 in IECs developed more tumors in the distal colon as well as a specific microbiota signature. Collectively, our results suggest that the Apc genetic status critically controls the effects of mitochondrial stress on intestinal tumor development.
2026-02-19 | PXD046922 | Pride