E-MTAB-6723
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6723 | ExpressionAtlas | 2018-06-04
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:To investigate the influence of Interleukin-22 (IL-22) on colonic intestinal stem cells, we assessed gene expression in these cells during homeostasis and after induction of DNA damage. IL-22 is a lymphocyte-derived cytokine that targets exclusively non-hematopoietic cells. The receptor is expressed on intestinal epithelial cells, including Lgr5+ stem cells. The colonic Lgr5+ epithelial stem cells were highly purified as DAPI-EpCam+CD45-CD24MedLgr5+. DNA damage was induced by whole body irradiation with 8 Gy and cells were isolated 24h after exposure. The following populations were analyzed: Wildtype, unirradiated (Ctrl) Il22-/-, unirradiated (Ctrl) Wildtype, 24h after 8Gy Il22-/-, 24h after 8Gy
2019-01-01 | E-MTAB-6723 | biostudies-arrayexpress
Project description:RNA Seq of colonic Lgr5+ epithelial stem cells in Il22+/+ and Il22-/- mice during homeostasis and 24h after irradiation with 8 Gy
| PRJEB26459 | ENA
Project description:<p>Pulmonary fibrosis is a heterogenous syndrome in which fibrotic scar replaces normal lung tissue. We performed massively parallel single-cell RNA-Seq on lung tissue from eight lung transplant donors and eight patients with pulmonary fibrosis. Combined with in situ RNA hybridization, with amplification, these data provide a molecular atlas of disease pathobiology. We identified a distinct, novel population of profibrotic alveolar macrophages exclusively in patients with fibrosis. Within epithelial cells, the expression of genes involved in Wnt secretion and response was restricted to non-overlapping cells. We identified rare cell populations including airway stem cells and senescent cells emerging during pulmonary fibrosis. Analysis of a cryobiopsy specimen from a patient with early disease supports the clinical application of single-cell RNA-Seq to develop personalized approaches to therapy.</p>
| phs001750 | dbGaP
Project description:The function of m6A modification in colonic epithelial cells has been validated in our study that depletion of METTL14 in colonic epithelial cells triggers cell death. To further explore the biological effects of m6A deficiency in colonic epithelial cell heterogeneity, we performed single cell RNA-seq of colonic epithelial cells form 2-week-old Mettl14-KO and WT control mice
2022-04-19 | GSE171422 | GEO
Project description:Ron (Mst1r), the receptor for MSP is highly expressed in colonic epithelial cells, especially in immature cell types, such as stem cells, TA cells and immature enterocytes. To identify genes that can be induced by MSP in mouse colonic epithelial cells, we performed bulk RNA-seq using day2 colon spheroids.
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Project description:Leber2015 - Mucosal immunity and gut
microbiome interaction during C. difficile infection
This model is described in the article:
Systems Modeling of
Interactions between Mucosal Immunity and the Gut Microbiome
during Clostridium difficile Infection.
Leber A, Viladomiu M, Hontecillas R,
Abedi V, Philipson C, Hoops S, Howard B, Bassaganya-Riera
J.
PLoS ONE 2015; 10(7): e0134849
Abstract:
Clostridium difficile infections are associated with the use
of broad-spectrum antibiotics and result in an exuberant
inflammatory response, leading to nosocomial diarrhea, colitis
and even death. To better understand the dynamics of mucosal
immunity during C. difficile infection from initiation through
expansion to resolution, we built a computational model of the
mucosal immune response to the bacterium. The model was
calibrated using data from a mouse model of C. difficile
infection. The model demonstrates a crucial role of T helper 17
(Th17) effector responses in the colonic lamina propria and
luminal commensal bacteria populations in the clearance of C.
difficile and colonic pathology, whereas regulatory T (Treg)
cells responses are associated with the recovery phase. In
addition, the production of anti-microbial peptides by inflamed
epithelial cells and activated neutrophils in response to C.
difficile infection inhibit the re-growth of beneficial
commensal bacterial species. Computational simulations suggest
that the removal of neutrophil and epithelial cell derived
anti-microbial inhibitions, separately and together, on
commensal bacterial regrowth promote recovery and minimize
colonic inflammatory pathology. Simulation results predict a
decrease in colonic inflammatory markers, such as neutrophilic
influx and Th17 cells in the colonic lamina propria, and length
of infection with accelerated commensal bacteria re-growth
through altered anti-microbial inhibition. Computational
modeling provides novel insights on the therapeutic value of
repopulating the colonic microbiome and inducing regulatory
mucosal immune responses during C. difficile infection. Thus,
modeling mucosal immunity-gut microbiota interactions has the
potential to guide the development of targeted fecal
transplantation therapies in the context of precision medicine
interventions.
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BIOMD0000000583.
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2014-04-08 | BIOMD0000000583 | BioModels
Project description:Analysis of the RNA-seq data performed in IR vs NIR hematopoietic stem cells show the loss of the TNF_via_NFKB signature. We showed that the loss of this signature could be associated with hematopoietic stem cell gene deregulation. To validate this association, we tested if TNFa treatment before irradiation was able to prevent IR-effect on HSC gene deregulation. For this purpose, we treated mice with TNFa 1h before irradiation (IR_TNF) and performed RNA-seq experiments on hematopoietic stem cells 1 month after irradiation and compared them to hematopoietic stem cells sorted from non irradiated mice (NIR) and from non-treated irradiated mice (IR).
2022-06-24 | E-MTAB-11867 | biostudies-arrayexpress
Project description:Colonic epithelial repair is a key determinant of health. After injury, repair initiates through phenotypic reprogramming of wounded epithelium to a regenerative state permissive for the activation of alternative stem cell populations and healing. Although cytokine signals such as interferon help induce regenerative reprogramming, the signals that modify this state as the wound resolves remain largely unknown. Here we show that, during healing, the late upregulation of a cytokine receptor, tumor necrosis factor (TNF) receptor 2 (R2, TNFR2, Tnfrsf1b), clears the phenotype of regenerative signaling and restores homeostatic patterns of epithelial differentiation. Mice lacking epithelial-specific expression of TNFR2 also failed to complete colon ulcer healing, suggesting that full repair requires coordination of both regenerative and homeostatic epithelial phenotypes. In single-cell RNA-seq experiments, we find that colonic epithelial organoids grown from Tnfr2-/- mice retain a highly enriched census of progenitor cells and reduced representation of differentiated cells, consistent with TNFR2's role in promoting differentiation. These results demonstrate how epithelial cells adapt to inflammatory cues to choreograph repair.
2023-08-22 | GSE230816 | GEO