Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1227685 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [30_week_Liver]
2014-09-08 | E-GEOD-58086 | ExpressionAtlas
Project description:Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences [8_week_ileal]
2014-09-08 | E-GEOD-58085 | ExpressionAtlas
Project description:Gene expression accompanying the promotion of hepatocellular carcinoma by intestinal microbiota and Tlr4 in mice.
2014-10-10 | E-GEOD-30485 | ExpressionAtlas
Project description:Interplay of host microbiota, genetic perturbations, and inflammation promote local development of intestinal neoplasms in mice
2019-05-14 | E-GEOD-47735 | ExpressionAtlas
Project description:Painong Powder, TCM, modulates gut microbiota imbalance in DSS-induced UC mice
| PRJNA725682 | ENA
Project description:Interventions: Control group A:Chemotherapy + probiotics;Control group B:Chemotherapy + Chinese Medicine;Treatment group:Chemotherapy + probiotics + Chinese medicine;Negative control group:None
Primary outcome(s): Intestinal microbiota detection;TCM symptom score and efficacy evaluation
Study Design: Parallel
| 83529 | ecrin-mdr-crc
Project description:Monosodium glutamate regulate intestinal microbiota
| PRJNA488680 | 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. 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:Circadian rhythmicity is a defining feature of mammalian metabolism that synchronizes metabolic processes to day-night light cycles. Here, we show that the intestinal microbiota programs diurnal metabolic rhythms in the mouse small intestine through histone deacetylase 3 (HDAC3). The microbiota induced expression of intestinal epithelial HDAC3, which was recruited rhythmically to chromatin and produced synchronized diurnal oscillations in histone acetylation, metabolic gene expression, and nutrient uptake. HDAC3 also functioned non-canonically to coactivate estrogen related receptor a (ERRa), inducing microbiota-dependent rhythmic transcription of the lipid transporter gene Cd36 and promoting lipid absorption and diet-induced obesity. Our findings reveal that HDAC3 integrates microbial and circadian cues to regulate diurnal metabolic rhythms, and pinpoint a key mechanism by which the microbiota controls host metabolism.
2019-09-26 | GSE134303 | GEO
Project description:Gut-brain connections monitor the intestinal tissue and its microbial and dietary content1, regulating both intestinal physiological functions such as nutrient absorption and motility2,3, and brain–wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microbes and relay this information to central nervous system (CNS) areas that, in turn, regulate gut physiology4. We characterized the influence of the microbiota on enteric–associated neurons (EAN) by combining gnotobiotic mouse models with transcriptomics, circuit–tracing methods, and functional manipulation. We found that the gut microbiome modulates gut–extrinsic sympathetic neurons; while microbiota depletion led to increased cFos expression, colonization of germ-free mice with short-chain fatty acid–producing bacteria suppressed cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling, and anterograde tracing identified a subset of distal intestine-projecting vagal neurons positioned to play an afferent role in microbiota–mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identified brainstem sensory nuclei activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota–dependent control of gut extrinsic sympathetic activation through a gut-brain circuit.
2020-03-20 | GSE145986 | GEO