Project description:This dataset consists of RNA-sequencing of intestinal organoids at rest and after stimulation with the TLR5 ligand flagellin for 4 hours. The goal of this study was to understand the differential patterns of gene expression induced upon stimulation with a TLR ligand in small intestine organoids, colon organoids, and organoids that had been skewed to generate a higher proportion of Paneth cells.
Project description:Analysis of gene expression in Caco-2 intestinal epithelial cells stimulated with flagellated or aflagellated S. enteritidis or recombinant flagellin. Results provide insight into how flagellin mediates innate immune responses in intestinal epithelial cells. Keywords: Gene expression analysis
Project description:Liver X Receptor (LXR) activation in intestinal epithelial organoids promotes their growth in vitro. To investigate the downstream effect of LXR activation in intestinal epithelial cells and identify potential pathways driving regeneration, we carried out an unbiased transcriptomic analysis of intestinal epithelial organoids stimulated with the LXR agonist GW3965. In detail, wild type small intestinal crypts were seeded in vitro and stimulated with vehicle (DMSO) or GW3965. After six hours, closing crypts (organoids) were collected for RNA extraction and were analyzed by RNA sequencing.
Project description:The purpose of this study was to characterise iPSC-derived human intestinal epithelial organoids (iPSCo) by comparing these cultures with primary purified intestinal epithelial cells (IEC). Intestinal epithelial organoid (IEO) cultures were derived from at least three different lines of iPSCs, RNA was extracted and gene expression was profiled using RNA-sequencing. We compared these profiles with datasets we have previously derived from purified IEC from mature terminal ileum (TI) and sigmoid colon (SC) as well as human fetal proximal gut (FPG) and fetal distal gut (FDG).
Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with interferon-gamma. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 1 ng/mL of recombinant mouse interferon-gamma protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.
Project description:We aimed to investigate gene expression changes in intestinal organoids from different mouse genotypes after treatment with TGF-beta. Wild-type, villinCreER;KrasG12D/+;Trp53fl/flRosa26N1icd/+ (KPN), and villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/flTgfbrIfl/fl (AKPT) intestinal organoids were plated, and the media was supplemented with 5ng/mL of recombinant mouse TGFß1 protein on Day 3. RNA was collected 24h later and processed for RNA sequencing.
Project description:To assess the role of LSD1 in mice small intestinal epithelium, small intestinal organoids were treated with an inhibitor for LSD1 (GSK-LSD1) and compared to untreated organoids. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, paneth cells dissappear upon GSK-LSD1 treatment. We used these sequencing data to show that these small intestinal organoids have a similar phenotype as mice epithelium without LSD1.
Project description:Bulk RNA sequencing was performed on intestinal and airway organoids. Also airway organoid derived air-liquid interface cultures were sequenced
Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we grew small intestinal organoids in vitro from mice with an epithelial specific deletion of LSD1 (Villin-Cre+; Lsd1f/f) and from wild type (Villin-Cre-; Lsd1f/f) mice. This experiment uses a new Cre strain with 100% recombination efficiency. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, Paneth cells are not present in LSD1-KO small intestinal organoids. We used these sequencing data to show intrinsic epithelial changes in the intestinal epithelium caused by LSD1 deletion in the absence of microbiota and surrounding in vivo cell types.