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Transcriptional profiling of murine small intestinal epithelial cells stimulated with interleukin-28A

ABSTRACT: Transcriptional profiling of murine small intestinal epithelial cells stimulated with interleukin-28A

PROVIDER: PRJEB14619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1474921.fastq.gz	Fastqsanger.gz
	ERR1474922.fastq.gz	Fastqsanger.gz
	ERR1474923.fastq.gz	Fastqsanger.gz
	ERR1474924.fastq.gz	Fastqsanger.gz
	ERR1474925.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of murine small intestinal epithelial cells stimulated with interleukin-28A

Project description:Organoids derived from small intestine epithelial cells of C57BL/6 wild-type mice were cultured in the presence or absence of IL-28 (1000 ng/ml) for 24 hours. The experimental setup included 8 samples in a pairwise design (4 unstimulated vs 4 stimulated). Profiling of whole-genome transcriptomic patterns was performed by RNA-Seq on an Illumina HiSeq 2500 platform using total RNA at the Next Generation Sequencing core unit of the University Hospital Erlangen, Germany. Demultiplexed reads were quality filtered against rRNAs, tRNAs, mt-rRNAs and mt-tRNAs. Alignment against the mus musculus reference genome (Ensemble V.84 for GRCm38) was performed with RNA-seq aligner STAR (V.2.5.1b) and statistical analysis of unique mappings (HTseq count) was computed in R using the DESeq2 1.10.1.

2017-07-01 | E-MTAB-4862 | biostudies-arrayexpress

Transcription profiling by array of human hepatic Huh7 cells stimulated with IL-28A or IL-29 compared to untreated cells

Project description:Aim of this study was to compare the effects of the lambda interferons IL-28A and IL-29 regarding transcriptional activation/repression of gene expression. For this purpose, the hepatic cell line Huh7 was stimulated with 100 ng/ml IL-28A or IL-29 for 6 hours or was left unstimulated. Then, gene expression of IL-28A or IL-29 treated cells was compared to expression in unstimulated cells

2011-11-22 | E-MEXP-2861 | biostudies-arrayexpress

Interleukin-28A maintains the intestinal epithelial barrier function through regulation of claudin-1.

Project description:BackgroundInterleukin-28A (IL-28A or interferon-λ2) is reported to maintain intestinal mucosal homeostasis. However, the effects and mechanisms of IL-28A on intestinal ischemia reperfusion (I/R) have not yet been studied.MethodsAdult C57BL/6 mice were randomly divided into three groups: sham, I/R, and I/R+IL-28A (n=5 in each group). The I/R+IL-28A group mice were injected with recombinant mouse IL-28A 12 hours before the operation. Mice were sacrificed 6 hours after reperfusion. The mucosal permeability was investigated, and histology analyses were performed. Additionally, a hypoxic Caco-2 cell culture model was established. Fludarabine was used to inhibit phosphorylated signal transducer and activator of transcription 1 (pSTAT1). The expression of IL-28A, tight junctions (TJs), and pSTAT1 was assessed by western blot, immunohistochemical (IHC) staining, or immunofluorescence staining. Epithelial permeability was measured by transepithelial electrical resistance (TER).ResultsThe expression of IL-28A was decreased in intestinal lamina propria in the I/R group compared with the control group. Administration of IL-28A significantly alleviated the I/R-induced increase in intestinal permeability and tissue damage. Treatment with IL-28A significantly attenuated intestinal I/R-induced disruption of TJ proteins, including zonula occludens-1 (ZO-1), occludin, and claudin-1. In vitro, IL-28A treatment reversed the decrease in TER of Caco-2 monolayers exposed to hypoxic environments. IL-28A led to the activation of STAT1 and the upregulation of claudin-1 expression both in vivo and in vitro. Also, inhibiting phosphorylation of STAT1 reversed the effects of IL-28A on the expression and distribution of claudin-1 in Caco-2 cells.ConclusionsIntestinal epithelial barrier dysfunction caused by intestinal I/R is ameliorated by IL-28A via the regulation of claudin-1.

| S-EPMC8033364 | biostudies-literature

Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.

Project description:Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.

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Methanocaldococcus sp. 28A isolate:28A

Project description:Methanocaldococcus sp. 28A isolate:28A Genome sequencing

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Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6

Project description:IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia. In this dataset, we include the expression data obtained from primary murine bone marrow-derived macrophages from control and IL6ralpha-deficient macrophages (n=4vs4) stimulated with interleukin-6 (IL-6)

2014-03-30 | GSE47426 | GEO

Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.

Project description:Previous stimulation experiments of stimulated primary murine colonic fibroblasts with IL-36R ligands for 4h in vitro showed an upregulation of pro-inflammatory cytokines e.g. IL-6, IL-1b and chemokines e.g. CXCL1, CCL2 indicating an important role for IL-36 in inflammation. We were interested in analyzing long-term stimulation (9 days) of intestinal fibroblasts to identify a putative differential expression profile. The experimental setup included 6 samples from 3 colons in a pairwise design (3 stimulated vs 3 unstimulated).

2018-11-19 | E-MTAB-6476 | biostudies-arrayexpress

Expression Data from murine control and IL6ralpha-deficient macrophages stimulated with Interleukin-6

2014-03-30 | E-GEOD-47426 | biostudies-arrayexpress

Murine small intestinal crypt cells: IGF-1 stimulated vs. control

2010-11-01 | GSE20133 | GEO

Murine small intestinal crypt cells: IGF-1 stimulated vs. control

Project description:microRNA profiling of mouse small intestinal crypt cells comparing control untreated with cells treated with insulin growth factor-1 (IGF-1). IGF-1 stimulated cell proliferation, as observed in Brdu incoporation assay. Two condition experiment. Control vs IGF-1 treatment. Biological replicates: 3 control, 3 treated. Independently grown and harvested. One replicate per array

2010-11-01 | E-GEOD-20133 | biostudies-arrayexpress

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