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Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [scRNAseq]

ABSTRACT: Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [scRNAseq]

PROVIDER: PRJNA768810 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16206635.fastq.gz	Fastqsanger.gz
	SRR16206636.fastq.gz	Fastqsanger.gz
	SRR16206637.fastq.gz	Fastqsanger.gz
	SRR16206638.fastq.gz	Fastqsanger.gz
	SRR16206639.fastq.gz	Fastqsanger.gz

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Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200211YilA]

Project description:Intestinal stem cells (ISCs) depend on niche factors for proper function. Here, we focus on RSPO3, an essential ISC niche factor, that engages the Lgr5 receptor on ISCs to potentiate WNT signaling, an interaction that is critical for maintaining intestinal stemness. Leveraging novel Rspo3-GFP and Grem1-tdTomato-CreERT2 genetically engineered mice together with single-cell mRNA profiling, we find that RSPO3 is expressed by lymphatic endothelial cells (LECs) and Rspo3+Grem1+ (RG) fibroblasts in the intestinal stroma where RG fibroblasts surround lymphatics and are in close proximity to Lgr5+ ISCs near the crypt base. Functionally, RG fibroblasts through the production of RSPO3 and GREM1 and LECs through the production of RSPO3 foster intestinal organoid propagation in vitro. Rspo3 loss in either or both of these niche cells in vivo compromises ISC numbers, villi length, and repair after irradiation-induced injury. Mechanistically, irradiation-induced damage expands LEC and RG fibroblast numbers and enhances the latters’ generation of RSPO3 through IL-1 receptor activation. We propose that LECs represent a novel component of the ISC niche, which together with RG fibroblasts, provide essential RSPO3 to sustain ISCs in homeostasis and regeneration.

2022-09-08 | GSE185348 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [scRNAseq]

2022-09-08 | GSE185354 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200909Yil]

2022-09-08 | GSE185350 | GEO

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury

Project description:Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury

| PRJNA768802 | ENA

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200909Yil]

Project description:Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200909Yil]

| PRJNA768809 | ENA

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200211YilA]

Project description:Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury [200211YilA]

| PRJNA768808 | ENA

Lymphatic endothelial cells, together with Rspo3+Grem1+ fibroblasts, support intestinal stem cells through the production of R-spondin3 in homeostasis and injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-08 | GSE185356 | GEO

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [Rspo3 KO]

Project description:We find that lymphatic Rspo3 is essential for intestinal regeneration after cytotoxic injury.

2022-07-18 | GSE198465 | GEO

Differential expression of mouse Grem1+ Vs. Grem1- bone-marrow cells

Project description:The gene expression of bone marrow cells of mice enriched for Gremlin1 vs control was measured (n=3). It is not known if endogenous adult mesenchymal stem cells (MSCs) exist.Following culture,perisinusoidal mesenchymal cells can clonally recapitulate the skeletal microenvironment, but this fails to confirm their endogenous lineage repertoire. Multipotential MSCs in vitro may be fate-restricted in vivo and specific perisinusoidal recombination does not trace bone or cartilage Reconciling in vitro MSCs with their in vivo potential has been challenging and remains untested outside of the bone. We prove that expression of the bone morphogenetic protein (BMP)-antagonist gremlin 1 (Grem1) identifies a population of self-renewing, multipotent bone, cartilage and stromal-primed MSCs in both health and healing that are completely distinct from the established Nes-GFP niche-supporting mesenchymal cells. Grem1 recombination also identifies small intestinal MSCs (siMSCs) that can be transplanted and clonally trace the self-renewing, multilineage periepithelial mesenchymal sheath. Our findings prove the existence of adult MSCs that are regionally and functionally distinct from perisinusoidal Nes-GFP cells. We also established that the mesenchyme undergoes ordered turnover outside of the bone and may help to preserve regional niches. Grem1 MSCs provide a new focus for investigating mesenchymal renewal and repair. a.Adult (6-8 weeks) Grem1;TdTomato mice were induced by oral tamoxifen and their bone marrow harvested by digestion sorted for Non-recombined CD45/CD31/Ter-119 triple negative bone marrow cells (n=3). b.Adult (6-8 weeks) Grem1;TdTomato mice were induced by oral tamoxifen and their bone marrow harvested by digestion sorted for Grem1 (n=3). Same mice as in a so that samples are matched.

2015-02-10 | E-GEOD-57729 | biostudies-arrayexpress

cis-regulation of Grem1 expression during limb development [ATAC HH24]

Project description:Spatiotemporal gene expression programs are orchestrated by transcriptional enhancers which interact with target-gene promoters to regulate gene expression. The BMP antagonist Gremlin1 (Grem1) is an important node in the gene regulatory network that controls vertebrate limb development. In this study, we used a combination of open chromatin profiling (ATAC-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) in mouse and chick to identify putative cis-regulatory modules (CRMs) that regulate Grem1 in limb buds. Using CRISPR/Cas genome editing we generated different Grem1 regulatory alleles lacking either individual CRMs, combinations or entire enhancer clusters. To study potential interactions of these CRMs with the Grem1 promoter, we generated 4C-seq profiles of specific regulatory alleles. Taken together our results revealed that the spatio-temporal changes in Grem1 expression are caused by cis-regulatory alterations due to the deletions of enhancer clusters rather than global changes in chromatin architecture.

2021-07-30 | GSE151467 | GEO

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