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Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

ABSTRACT: To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR.

ORGANISM(S): Mus musculus

PROVIDER: GSE35651 | GEO | 2015/02/08

SECONDARY ACCESSION(S): PRJNA152421

REPOSITORIES: GEO

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Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

Project description:To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR. Colitis was induced with 3% DSS, 36,000-50,000 M.W. (MP Biomedicals,) in the drinking water for 3 days. Genes responsible for DSS treatment in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-02-08 | E-GEOD-35651 | biostudies-arrayexpress

Whole ileal tissue from day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+/- mice

Project description:Total RNA sequencing (RNA-seq) of the terminal ileum of day 6 Dextran Sodium Sulfate (DSS) administered Il17rafl/fl;Atoh1-cre+ mice and littermate cre- mice was performed.

2022-01-25 | GSE189219 | GEO

RNA-Seq of wild type and somatostatin 3 CrispR/Cas9 zebrafish mutants treated with dextran sodium sulfate (DSS)

Project description:Wild type and somatostatin 3 (Sst3) gene CrispR/Cas9 mutants of the AB zebrafish strain were treated with dextran sodium sulfate (DSS) to determine the role of sst3 in the innate immune response.

2020-07-31 | E-MTAB-9018 | biostudies-arrayexpress

Transcriptomic anlaysis of the early response of the colonic epithelium to colitis induction by dextran sodium sulfate (DSS)

Project description:We compared the transcriptional signatures of the colonic mucosa from control mice (WT) versus mice deficient for the epithelial pantetheinase Vnn1 (Vnn1KO) or overexpressing Vnn1 specifically in intestinal epithelial cells (VIVA transgenic mice), during the development of DSS-induced colitis.

2022-11-24 | GSE174166 | GEO

A super carbonate apatite (sCA) could deliver sufficient amounts of miRNA into the colorectum inflamed by dextran sodium sulfate (DSS) treatment

Project description:Purpose: A super carbonate apatite (sCA) nanoparticle is an in vivo pH-sensitive delivery system for siRNA and microRNA. These carriers accumulate specifically in tumors, yet they cause no serious adverse events in mice and monkeys. Systemic administration of sCA incorporating siRNA and microRNA has demonstrated superb tumor suppressive effects in vivo. We recently observed that sCA could deliver abundant nucleic acids to the inflammatory sites in rheumatoid arthritis mouse model. Based on the success, we tried to examine whether sCA could deliver sufficient amounts of miRNA into the colorectum inflamed by dextran sodium sulfate (DSS) treatment. Methods: We performed a RNA sequencing analysis of the DSS-treated colon walls. DSS was administered for 4 days and sCA-miR-29a, sCA-miR-29b, sCA-NC-miR was injected on days 1, 2, 3. On day 4, colorectum was removed and the mRNA samples were subject to the RNA sequencing analysis. Results: RNA sequencing of the rectum samples showed a number of enhanced or reduced gene expression in DSS treated NC-miR group on day 4 compared to normal mice. Such tendency of upregulation or downregulation was also noted in DSS-treated NC-miR group on day 2. Comparison of DSS treated samples on day 4 among NC-miR, miR-29a and miR-29b groups, revealed that several gene expression related to the interferon pathway was reversed by miR-29a or miR-29b towards the normal controls. These include Stat1, Stat2, IRF7, IRF9, and IFIT1. Conclusions: Many molecules in the interferon signaling pathway were activated in DSS-induced colitis on day 4 and Stat1, Stat2, IRF7, IRF9, and IFIT1 were key molecules in the interferon related pathways. These findings suggest that sCA-miR-29a or sCA-miR-29b may inhibit type 1 IFN and type 2 IFN pathways which are otherwise activated by DSS treatment.

2018-08-10 | GSE93162 | GEO

Effect of colonic epithelial knockout of tumor necrosis factor receptor 2 (TNFR2) in dextran sulfate sodium (DSS)-induced colitis

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 interferons may help induce regenerative reprogramming, the signals that modify this state as the wound resolves remain largely unknown. Here we examined whether cytokine signaling mediated by tumor necrosis factor receptor 2 (TNFR2) influenced the wound repair process. We examined mice with targeted deletion of the Tnfrsf1b (TNFR2) gene in intestinal/colonic epithelium (Vil1::Cre;Tnfr2-f/f) and compared their transcriptional profiles to control (Tnfr2-f/f) mice. We sorted EpCAM+ (epithelial) cells from Vil1::Cre;Tnfr2-f/f and control DSS-treated mice and performed bulk RNA-Seq. Comparison of transcript expression profile before and after DSS-induced colitis in control (Tnfr2-f/f) mice revealed upregulation of pathways associated with metabolic regulation, ribosomal function, oxidative stress, TNF signaling, and focal adhesions after DSS treatment. Pathway enrichment analysis demonstrated elevated regenerative (“fetal”) intestinal signaling, reduced inflammation, and increased proliferative signaling in Vil1::Cre;Tnfr2-f/f colonic epithelium after DSS treatment. The knockout epithelium also showed reduced expression of markers of differentiated colonic epithelium and elevated expression of progenitor cell signaling. Thus, the transcriptional data were consistent with increased regenerative signaling in TNFR2-knockout epithelium, suggesting that TNFR2 has a role in restraining the relatively undifferentiated regenerative state.

2023-08-22 | GSE230329 | GEO

Luminal metabolome profiles of mice developed dextran sulfate sodium (DSS) colitis

Project description:Luminal (cecal) metabolome of DSS-colitis mice and control mice were compared.

2019-09-12 | ST001250 | MetabolomicsWorkbench

Gene Array Analysis of Methylthioadenosine Supplementation in Dextran Sulfate Sodium Induced Colitis

Project description:Study hypothesized that oral supplementation of methylthioadenosine (MTA) would reduce the inflammatory response in mice exposed to an agent that induces colitis (DSS) and that this reduction in inflammatory response would lead to reduced clinical disease burden. Total RNA was collected from isolated colons of mice in the following treatment groups: untreated controls, DSS only, DSS+MTA

2011-12-20 | E-GEOD-34553 | biostudies-arrayexpress

Uridine Ameliorates Dextran Sulfate Sodium (DSS)-Induced Colitis in Mice.

Project description: Not available

| S-EPMC5478663 | biostudies-literature

Mechanisms research on Cyanidin-3-O-glucoside ameliorating dextran sulfate sodium (DSS)-induced colitis.

Project description:TMT proteomics for colonic mucosa in DSS-induced colitis mice with or without administrated Cyanidin-3-O-glucoside was used for discovery of differential expressed proteins.

2023-07-10 | PXD043662 | iProX

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