Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA114251 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE12997: Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium GSE12998: Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium after O157 infection Refer to individual Series
2011-01-27 | E-GEOD-13061 | biostudies-arrayexpress
Project description:A huge number of microorganisms are colonized in human gut and the balance of their composition is closely related to human health. Recently, many probiotics such as bifidobacteria or lactobacilli have been introduced in our life as effective agents. However, we have not well understood their beneficial mechanisms including host-bacterial crosstalk To analyze the differences of gene expression between BA- or BL-associated murine colonic epithelium, we performed comparative transcriptomic analysis. Bifidobacterium adolescentis (BA)-associated mice and Bifidobacterium longum (BL)-associated mice were used. Colonic epithelium was isolated and gene expression profile was analyzed. Each 3 samples were analyzed.
2011-01-27 | E-GEOD-12997 | biostudies-arrayexpress
Project description:Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium after O157 infection
| PRJNA114253 | ENA
Project description:A huge number of microorganisms are colonized in human gut and the balance of their composition is closely related to human health. Recently, many probiotics such as bifidobacteria or lactobacilli have been introduced in our life as effective agents. However, we have not well understood their beneficial mechanisms including host-bacterial crosstalk To analyze the differences of gene expression between BA- or BL-associated murine colonic epithelium, we performed comparative transcriptomic analysis.
2011-01-27 | GSE12997 | GEO
Project description:Transcriptional profiling of microscopically laser dissected murine colonic tissue from 3 separate normal crypts, wound associated epithelium (WAE), normal epithelium, and regenerating crypts (day 6 only) at days 2,4,and 6 after colonic mucosal injury. Injury model performed as described in: H. Seno et al., Efficient colonic mucosal wound repair requires Trem2 signaling. Proc. Natl. Acad. Sci. USA 106, 256-261 (2009)
2012-06-18 | E-MTAB-1175 | biostudies-arrayexpress
Project description:Colonic goblet cells respond to invading enteropathogens by secreting Muc2 mucin and other specific goblet cell proteins that physically entrap and expel microbes away from the epithelium. At present, it is unclear how innate effectors in the gut, including small cationic cathelicidin peptides secreted by the intestinal epithelium and leukocytes, contribute to mucus barrier defense during infections. In this study, we used cathelicidin-deficient (Camp-/-) mice, colonoids, and human colonic LS174T goblet cells to elucidate the mechanisms by which cathelicidin regulates goblet cell secretions in innate host defense against attaching/effacing Citrobacter rodentium. We showed that even though Camp-/- littermates infected with C. rodentium displayed increased fecal shedding and epithelial colonization, Muc2 mucin granules were retained in bloated colonic goblet cells that impaired mucus secretion and expressed less mucus-associated proteins, as quantified by proteomic analysis. C. rodentium infected Camp-/- littermates showed impaired reactive oxygen species (ROS) production and transcriptomic profiling associated with decreased ROS biosynthesis and an increase in ROS negative regulators. Camp-/- bone marrow derived macrophages produced less ROS than their wild-type counterparts. In LS174T goblet cells, human cathelicidin LL-37 promptly induced the secretion of goblet cell-associated TFF3 and RELMβ, which was dependent on ROS production. These findings demonstrate that cathelicidin signaling in colonic goblet cells regulates mucus and mucin-associated protein secretion via an ROS-dependent mechanism to clear bacterial infections and restore gut homeostasis.
2023-05-04 | PXD041957 | Pride
Project description:Purpose: to determine cellular heterogeneity of the murine colonic epithelium and mesenchyme; Summary: We determined 16 disctinct sub-populations of colonic epithelial and mesenchymal cells. Further we found 3 distinct sub-populations of colonic PdgfraEGFP-positive fibroblasts.
2020-11-19 | GSE151257 | GEO
Project description:In Burkitt lymphoma (BL), an aggressive germinal-center (GC) derived non-Hodgkin B-cell lymphoma characterized by MYC translocations as early transforming event, the apoptotic properties of MYC must have been overcome by pro-survival signals. Whereas activation of the pro-survival factor NFkappaB is not eminent in BL, PI3K signalling, which mediates B cell receptor associated survival signals in mature B cells, might be the cooperating event. Here we prove this hypothesis by the generation of BL in mice upon concordant expression of MYC and activation of PI3K in GC B cells. Unlike existing murine BL-like models, our tumour model fully phenocopies primary human BL and reflects the complexity of the disease with regard to histological appearance, surface marker expression, and characteristic gene expression profiles. Like in human BL, tumour monoclonality indicated a multistep pathogenesis underlining MYC and PI3K as predisposing events that invariably lead to GC-derived BL formation. In accordance, copy number alteration analysis revealed genomic regions involved in BL pathogenesis. All samples were obtained from murine lymphomas (Cgamma1-cre; R26StopFLMYC;R26StopFLP110* animals). Cells used for microarray analysis were sorted reporter positive cells. Tumour cells were compared to a matched germline DANN sample to identify acquired aberrations.
2012-08-13 | E-GEOD-35219 | biostudies-arrayexpress
Project description:SARS-CoV-2 induces widespread transcriptomic changes in host cells upon infection, in part through activation and modulation of innate immunity pathways and downstream gene regulation. However, the mechanisms by which SARS-CoV-2 and its evolutionary variants differentially affect host cell transcriptomic states remain largely unclear. Through chromatin proteomic (iDAPT-MS) analysis, we found that although SARS-CoV-2 and other pathogenic coronaviruses exhibit similar proteomic shifts on chromatin, SARS-CoV-2 uniquely promotes TP53 nuclear accumulation and activation. Parallel assessment of SARS-CoV-2 viral protein expression on host chromatin states (ATAC-seq) identifies intracellular spike protein as a key determinant of virus-mediated chromatin accessibility changes. Multilevel chromatin profiling reveals increased TP53 nuclear accumulation, TP53-associated chromatin accessibility changes, and TP53 target gene activation upon expression of SARS-CoV-2 alpha (B.1.1.7) and delta (B.1.617.2) spike variants relative to the ancestral spike sequence. TP53, ACE2, and furin cleavage are required for these changes, driving decreased cellular proliferation, increased cellular senescence, and increased cytokine release. Finally, BA.1 but not BA.2, BA.2.12.1, nor BA.4/BA.5 spike expression leads to attenuated TP53 activity and fusogenicity relative to ancestral spike. Our findings implicate spike-mediated host TP53 activation as a “rheostat” of COVID-19 pathogenicity.
2023-09-09 | PXD034648 | Pride