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ABSTRACT: RNA-Seq of colonic epithelial cells in Fam3D KO mice

PROVIDER: PRJNA641502 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12079318_1.fastq.gz	Fastqsanger.gz
	SRR12079318_2.fastq.gz	Fastqsanger.gz
	SRR12079319_1.fastq.gz	Fastqsanger.gz
	SRR12079319_2.fastq.gz	Fastqsanger.gz
	SRR12079320_1.fastq.gz	Fastqsanger.gz

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m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [scRNA-seq]

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

RNA-seq data of intestinal epithelial cells and lamina propria dendritic cells

Project description:We report that Klebsiella pneumoniae promote Th1 cell induction in colon. To examine the influence of Klebsiella on colonic epithelial cells (ECs) and lamina propria CD11c+ dendritic cells (DCs), we performed RNA seq on them. Germ free mice were orally inoculated with Kp-2H7 or BAA-2552 and total RNA was isolated from colonic ECs and DCs 1 week after inoculation. Furthermore, we examined the involvement of TLRs in induction of Th1 cells using Myd88 KO, Trif KO, Myd88/Trif DKO mice. These deficient germ free mice were orally inoculated with Kp-2H7 and total RNA was isolated from colonic ECs 3 weeks after inoculation.

2017-10-20 | GSE101678 | GEO

Single-cell RNA Sequencing (scRNA−seq) Identifies L1CAM as a Key Mediator between Epithelial Tuft Cell and Innate Lymphoid Cell in the Colon of Hnrnp I Knockout Mice

Project description:(1) Background: Knockout (KO) of heterogeneous nuclear ribonucleoprotein I (Hnrnp I) in mouse intestinal epithelial cells (IECs) induced a severe inflammatory response in the colon, followed by hyperproliferation. This study aimed to investigate the epithelial lineage dynamics and cell–cell communications that underlie inflammation and colitis. (2) Methods: Single cells were isolated from the colons of wildtype (WT) and KO mice and used in scRNA−seq. Whole colons were collected for immunofluorescence staining and cytokine assays. (3) Results: from scRNA−seq, the number of DCLK1 + colonic tuft cells was significantly higher in the Hnrnp I KO mice compared to the WT mice. This was confirmed by immunofluorescent staining of DCLK1. The DCLK1 + colonic tuft cells in KO mice developed unique communications with lymphocytes via interactions between surface L1 cell adhesion molecule (L1CAM) and integrins. In the KO mice colons, a significantly elevated level of inflammatory cytokines IL4, IL6, and IL13 were observed, which marks type−2 immune responses directed by group 2 innate lymphoid cells (ILC2s). (4) Conclusions: This study demonstrates one critical cellular function of colonic tuft cells, which facilitates type−2 immune responses by com-municating with ILC2s via the L1CAM–integrins interaction. This communication promotes pro−inflammatory signaling pathways in ILC2, leading to the increased secretion of inflammatory cytokines.

2023-10-14 | GSE245188 | GEO

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [bulkRNA-seq]

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 cells, we performed RNA sequencing analysis of colonic epithelial cells form 2-week-old Mettl14-KO and WT control mice.The bioinformatic analysis revealed that METTL14 depletion increased the mRNA expression of NF-kB inhibitor Nfkbia, which favored TNF-induced cell death.

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RNA-sequencing analysis of colon RNA from mice with compound mutations of XBP1, caspase-8, TNFR1 and MLKL.

Project description:To purpose of this study was to assess how intestinal epithelial cell (IEC)-specific ablation of XBP1 or caspase-8 alone or in combination affected mucosal immune homeostastis and inflammation, and the role of TNFR1 and MLKL in the associated phenotypes. First, expression of colonic RNA from mice with combined IEC-specific XBP1 and caspase-8 ablation (Xbp1IEC-KO Casp8IEC-KO) was compared with Casp8IEC-KO, Xbp1IEC-KO, and wild-type mice. In addition, Xbp1IEC-KO Casp8IEC-KO Mlkl-/- and Xbp1IEC-KO Casp8IEC-KO Tnfr1IEC-KO mice were compared with Xbp1IEC-KO Casp8IEC-KO, Casp8IEC-KO, Xbp1IEC-KO as well as wild-type control mice. For each mouse line 5 individual mice were analysed.

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RNA-seq data of intestinal epithelial cells

Project description:We report that adhesion of microbes to intestinal epithelial cells is a critical cue for Th17 induction. SFB colonized in the intestine of mice can adhere to mouse small intestinal epithelial cells and induce intestinal Th17 cells. However, SFB colonized in rats cannot adhere to mouse intestinal epithelial cells and induce Th17 cells. Likewise, Citrobacter rodentium (WT) can adhere to mouse colonic epithelial cells and induce Th17 cells, but non-adherent mutant of C. rodentium (Δeae) cannot induce Th17 cells. To examine the influence of adherent bacteria on intestinal epithelial cells, we performed RNA seq. Germ free mice were orally inoculated with M-SFB or R-SFB and total RNA was isolated from small intestinal epithelial cells 1 week after inoculation. Alternatively, germ free mice were orally inoculated with C. rodentium WT or eae mutant and total RNA was isolated from colonic epithelial cells 5 days after inoculation. The gene expression of small intestinal epithelial cells isolated from small intestine of germ free mice (2 mice), mice monocolonized with M-SFB (2 mice) or R-SFB (3 mice), and colon of germ free mice (3 mice), mice monocolonized C. rodentium WT (3 mice) or eae mutant (3 mice).

2015-09-24 | E-GEOD-71734 | biostudies-arrayexpress

Mitochondrial perturbation in the intestine causes microbiota-dependent injury and gene signatures discriminative of inflammatory disease

Project description:Single-cell RNA-sequencing (scRNA-seq) data was generated from colonic tissue from Hsp60Δ/ΔIEC and Hsp60fl/fl mice at day 8 enriched in intestinal epithelial cells (IECs).

2024-07-10 | E-MTAB-14206 | biostudies-arrayexpress

RNA-seq data of intestinal epithelial cells

2015-09-24 | GSE71734 | GEO

The impact of dietary cellulose on transcriptional profiles of colonic epithelial cells during inflammation.

Project description:Purpose: Although dietary cellulose is considered health promoting, there is still a lack of understanding of cellular and molecular mechanisms. The aim of this study was to shed light on possible effects of the fiber on key players in intestinal homeostasis, including intestinal epithelial cells. Method: Mice were fed a diet containing cellulose as the only source of fiber (CD, control diet) or a fiber free diet (FFD, fiber-free diet) for four weeks and then treated with dextran sulphate sodium in the drinking water for five days. To ensure that gene signatures were derived from colonic epithelial cells and not from contaminating lymphocytes, RAG1 KO mice deficient in intraepithelial lymphocytes were used. Results: The analysis of differential expressed genes of colonic epithelial cells revealed multiple effects of dietary cellulose on the transcriptional profiles. In addition, cellulose caused a distinct clustering when comparing signature genes of different epithelial cell types. Conclusion: This study demonstrated that dietary cellulose impacts transcriptional programs in colonic epithelial cells during inflammation.

2021-05-31 | GSE151136 | GEO

RNA-seq analysis of colonic intestinal epithelial cells (IECs) isolated from naive wild-type C57BL/6 mice, DSS-treated wild-type C57BL/6 mice, Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion

Project description:The aim of this study is to compare the transcriptomic profile of colonic intestinal epithelial cells (IECs) at steady-state, and in several models of colitis: in naive wild-type C57BL/6 mice, in wild-type C57BL/6 mice treated for 7 days with 3% dextran sodium sulfate (DSS) in drinking water, in Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion. Colonic IECs were isolated and FACS-sorted, then subjected tu bulk RNA-seq.

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