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RNA-seq analysis of sorted colon epithelial cells and colon lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

ABSTRACT: RNA-seq analysis of sorted colon epithelial cells and colon lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

PROVIDER: PRJNA734517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14711064.fastq.gz	Fastqsanger.gz
	SRR14711065.fastq.gz	Fastqsanger.gz
	SRR14711066.fastq.gz	Fastqsanger.gz
	SRR14711067.fastq.gz	Fastqsanger.gz
	SRR14711068.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

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RNA-seq analysis of sorted colon epithelial cells and colon lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:The intestinal epithelium has a high turnover and constantly renews itself through proliferation of intestinal crypt cells, which depends on insufficiently characterized signals from the microenvironment. Here we show that colonic macrophages were located directly adjacent to epithelial crypt cells in mice, where they metabolically supported epithelial cell proliferation in an mTORC1-dependent manner. Specifically, mTORC1 activation in macrophages protected against colitis-induced intestinal damage and induced the synthesis of the polyamines spermidine and spermine. Epithelial cells ingested these polyamines and rewired their cellular metabolism for optimizing proliferation and defense. Notably, spermine directly stimulated proliferation of colon epithelial cells and colon organoids. Genetic interference with polyamine production in macrophages altered global polyamine levels in the colon and modified epithelial cell proliferation. Our results suggest that macrophages act as “commensals” that provide metabolic support to promote efficient self-renewal of the colon epithelium.

2023-08-08 | GSE175992 | GEO

scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

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RNA-seq analysis of sorted duodenum epithelial cells and duodenum lamia propria macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE196815 | GEO

scRNA-seq analysis of duodenum CD68+ macrophages from mice where Tsc2 is deleted in Lyz2-expressing cells

Project description:Iron is an essential cellular trace element and important for many physiological functions including erythropoiesis and host defense. It is taken up from the diet in the duodenum, the first part of the small intestine by enterocytes and loaded onto transferrin, the main iron transport molecules in the circulation. Macrophages are ancient sentinel cells that are implicated in all steps of systemic iron metabolism except duodenal iron import. By assessing mice that harbor a macrophage-specific deletion of the tuberous sclerosis complex 2 (Tsc2), a negative regulator of mTORC1, we found that these mice possessed various defects in iron metabolism including defective steady state erythropoiesis and a highly reduced saturation of transferrin with iron. This iron-deficiency phenotype was caused by a block of iron import from the duodenal epithelial cells into the circulation. Activation of mTORC1 in villous duodenal CD68+ macrophages induced expression of serine proteases and promoted local degradation of the major iron transport molecule transferrin, whereas depletion of macrophages in mice increased transferrin levels in the duodenal villi. Inhibition of serine protease activity restored transferrin levels in the Tsc2-deficient mice. Physiologically, transferrin levels were regulated in the villi during Citrobacter rodentium infection in mice. These data show that transferrin is controlled locally in the duodenum and establish macrophages as regulators of duodenal iron uptake.

2023-06-08 | GSE197175 | GEO

RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

Project description:RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

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RNA-seq analysis of FACS-sorted control and Tsc2-deleted nociceptors

Project description:The goals of this study are to compare the transcriptomes of control heterozygous and Tuberous sclerosis 2 (Tsc2) homozygous nociceptors that have been enriched by fluorescence-associated cell sorting (FACS) with the aim of identifying differences in genes associated with sensory behavior. Nav1.8-Cre transgenic mice were used to delete Tsc2 as well as express Green fluorescent protein from the Rosa26 locus. Tsc2 deletion constitutively activates mTORC1 signaling cell autonomously. Dissociated dorsal root ganglia from adult mice were FACS-sorted for GFP and analyzed by RNA-seq. We find that a number of sensory behavior associated genes are affected by Tsc2 deletion including Calca, Ntrk1, Mrgpra3, and Nppb. Additionally, profiling of ion channel expression showed a reduction in almost half of expressed sodium, potassium and calcium channel as well as G-protein coupled receptors. Other categories of genes such as transcription factors and ligand-gated ion channels contained an even numbers of up- and downregulated genes with many that did not change as a result of Tsc2 deletion. In addition, expression of most marker genes enriched in Isolectin B4 (IB4) negative neurons were strongly reduced in Tsc2 mutant nociceptors, consistent with reduced sensitivity to heat, which is a modality related to these neurons. We conclude Tsc2 deletion and consequent mTORC1 activation alters gene expression of nociceptors resulting in altered sensory thresholds.

2018-04-01 | GSE112499 | GEO

Expression profiles of CD45+ cells in colon lamina propria from macrophage-specific E4BP4 transgenic mouse

Project description:Purpose: The goals of this study are to confirm the hypothesis that E4BP4 regulates colon specific anti-inflammatory macrophage. Methods: We generated transgenic mice (TG) with macrophage-specific E4BP4 overexpression. CD45+ cells in colon lamina propria were isolated at Zeitgeber Time (ZT) 0 from TG mice and WT littermates during the recovery period of dextran sulfate sodium (DSS)-induced colitis, and total RNA was extracted. CD45+ cells in colon lamina propria RNA profiles were generated by deep sequencing for two groups with one mouse sample each. Results: There were significant differences between TG and WT mice. Conclusions: E4BP4 increased the number of M2 macrophage population and upregulated anti-inflammatory genes.

2024-03-31 | GSE183529 | GEO

Spatially separated intraepithelial and lamina propria neutrophils present distinct functional identities in the inflamed colon mucosa

Project description:We used GeoMx DSP technology to profile the gene expression information of intraepithelial neutrophils (IENs) and lamina propria neutrophils (LPNs) from moderate-severe UC patients's colon.

2025-03-10 | GSE289035 | GEO

Gene expression profiling of mT/mG;Lyz2.Cre vs IKKbetaf/f;Lyz2.Cre mouse bone marrow derived macrophages

Project description:Gene expresion comparison between tomato Lyz2 Cre and IKKbeta flox/flox Lyz2 Cre bone marrow derived macrophages

2019-06-28 | GSE94880 | GEO