GEO DataSets

(Submitter supplied) Background and aims: Current management of inflammatory bowel disease (IBD) leaves a clear unmet need to treat the severe epithelial damage. Modulation of Wnt signaling might present an opportunity to achieve histological remission and mucosal healing when treating IBD. Exogenous R-spondin (RSPO), which amplifies Wnt signals by maintaining cell surface expression of Frizzled (FZD) and low-density lipoprotein receptor-related protein (LRP) receptors, helps repair intestine epithelial damage, but it also induces hyperplasia of normal epithelium. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

16 Samples

Download data: TSV

(Submitter supplied) To further understand different gene expression of miR-31 knockout mouse colon and normal colon, we have employed colonic epithelium microarray expression profiling as a discovery platform to identify different genes with miR-31 knockout mouse colon and normal colon.comparision with normal colonic epithelium,upgene is 285 and downgene is 178 in knockout group.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL21163

6 Samples

Download data: TXT

(Submitter supplied) To define the mechanisms that underlie regeneration driven by EP4+ macrophages, we transcriptionally compared the WT and Csf1r-EP4-/- mature macrophages isolated from colon by 39 days post DSS treatment.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

11 Samples

Download data: TXT

(Submitter supplied) Wnt ligands oligomerize Frizzled (Fzd) and Lrp5/6 receptors to control the specification and activity of stem cells in many species. How Wnt is selectively activated in different stem cell populations, often within the same organ, is not understood. In lung alveoli, wherein Wnt-dependent epithelial and stromal progenitors are intermingled, we show that distinct Wnt receptors are expressed by epithelial (Fzd5/6), endothelial (Fzd4), and stromal (Fzd1) cells. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

18 Samples

Download data: TAB

(Submitter supplied) To investigate the detailed molecular mechanisms for the regulatory role of HIF-2α in experimental colitis, microarray gene expression analysis was performed on colon RNA isolated from 6- to 8-week-old Hif-2αF/F, Hif-2αlΔIE mice treated with 3%DSS for 3 days. Background & Aims: Hypoxic inflammation is characterized by decreased oxygen tension in inflammatory foci, and is a notable feature in inflammatory bowel disease (IBD). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

2 Samples

Download data: CEL

(Submitter supplied) Mucosal healing is a key treatment goal for inflammatory bowel disease, and epithelial regeneration is required for an intact gut epithelium. Long noncoding RNAs are involved in the development of inflammatory bowel disease. Here, we investigated the role of a novel long noncoding RNA, Gm31629, in epithelial regeneration. We used RNA-seq to to detail the global programme of gene expression in distal colon tissues from WT and Gm31629-/-.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

6 Samples

Download data: TXT

(Submitter supplied) We had one goal to perform this study: DSS-induced colitis receiving Sulfasalazine and Berberine colonrectum Transcriptomes

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL23479

6 Samples

Download data: XLS

(Submitter supplied) We had three goals to perform this study: compare normal mice and colitis mice，compare berberine effect in normal mice and compare berberine effect in colitis mice

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL23479

12 Samples

Download data: CSV

(Submitter supplied) Background & Aims Activation of the transcription factor nuclear factor-κB (NF-κB) has been associated with the development of inflammatory bowel disease (IBD). Copper metabolism MURR1 domain containing 1 (COMMD1), a regulator of various transport pathways, has been shown to limit NF-κB activation. We investigated the roles of COMMD1 in the pathogenesis of colitis in mice and IBD in human beings.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11202

12 Samples

Download data: TXT

(Submitter supplied) Chronic injury and inflammation pose high risks for epithelial dysplasia and cancer. In the “field cancerization” model, spontaneous mutations confer a stem-cell fitness advantage and promote gradual clonal expansion. Here, through 3d imaging, fate-mapping, biophysical modeling, and single-cell transcriptomics in a mouse model of acute colitis, we define an alternate, rapid mechanism for clonal expansion: the neutral activation of metabolically reprogrammed “founder progenitor cells” (FPCs) during wound healing. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

11 Samples

Download data: MTX, TXT

(Submitter supplied) The colonic epithelium can undergo multiple rounds of damage and repair, often in response to excessive inflammation. Our understanding of how this process occurs is limited by a lack of in vitro models that recapitulate key aspects of in vivo responses. We established a long-term, self-organizing 2D epithelial monolayer system to model the cyclic nature of epithelial alterations during injury-repair. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

31 Samples

Download data: TXT

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

4 Samples

Download data: MTX, TXT

(Submitter supplied) 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. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: CSV

(Submitter supplied) The early phase of colonic epithelial wound healing involves cellular reprogramming to a fetal-like state and reorganization of discrete crypt units into merged wound channels. After re-epithelialization is complete, a latter phase restoring homeostatic signaling and crypt patterning must occur. However, the signals that mediate this regenerative transition are unknown. Here we show that injury-associated upregulation of a cytokine receptor, tumor necrosis factor (TNF) receptor 2 (R2, TNFR2, Tnfrsf1b), suppresses fetal-like signaling and promotes crypt production. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

20 Samples

Download data: CSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

38 Samples

Download data

(Submitter supplied) Inflammation has long been recognized to contribute to cancer development, particularly across the gastrointestinal tract. Patients with inflammatory bowel disease have an increased risk for bowel cancers, and it has been posited that a field of genetic changes may underlie this risk. Wnt pathway alterations are infrequent, and our data suggest transcriptional rewiring away from Wnt. These findings suggest neoplastic bowel lesions developing in a background of inflammation experience lineage plasticity away from Wnt activation early during tumorigenesis and largely occur as genetically independent events. 

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

9 Samples

Download data: XLSX

(Submitter supplied) Inflammation has long been recognized to contribute to cancer development, particularly across the gastrointestinal tract. Patients with inflammatory bowel disease have an increased risk for bowel cancers, and it has been posited that a field of genetic changes may underlie this risk. Wnt pathway alterations are infrequent, and our data suggest transcriptional rewiring away from Wnt. These findings suggest neoplastic bowel lesions developing in a background of inflammation experience lineage plasticity away from Wnt activation early during tumorigenesis and largely occur as genetically independent events. 

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

11 Samples

Download data: XLSX

(Submitter supplied) Inflammation has long been recognized to contribute to cancer development, particularly across the gastrointestinal tract. Patients with inflammatory bowel disease have an increased risk for bowel cancers, and it has been posited that a field of genetic changes may underlie this risk. Wnt pathway alterations are infrequent, and our data suggest transcriptional rewiring away from Wnt. These findings suggest neoplastic bowel lesions developing in a background of inflammation experience lineage plasticity away from Wnt activation early during tumorigenesis and largely occur as genetically independent events. 

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

18 Samples

Download data: TXT