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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE198465 | GEO | 2022/07/18

REPOSITORIES: GEO

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Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury [endothelial cells]

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

2022-07-18 | GSE198468 | GEO

Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury

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

2022-07-18 | GSE198469 | GEO

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

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 | 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 [200211YilA]

2022-09-08 | GSE185348 | GEO

Targeting PTPRK-RSPO3 tumors

Project description:Targeting PTPRK-RSPO3 colon tumors.

| PRJEB10684 | ENA

Identification of endothelial genes co-regulated upon endothelial Evi/Wls and Rspo3 deletion

Project description:Inducible endothelial Rspo3 deletion resulted in perturbed developmental and tumor vascular remodeling. Rspo3-iECKO mice strikingly phenocopied the non-canonical WNT signaling-induced vascular defects of mice deleted for the WNT secretion factor Evi/Wls. An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified novel target genes, which could be linked to WNT/Ca2+/NFAT signaling. In summary, the study identifies endothelial RSPO3-driven non canonical WNT/Ca2+/NFAT signaling as critical maintenance pathway of the remodeling vasculature.

2016-02-03 | GSE75836 | GEO

Gastric Lgr5+ cells are programmed by Rspo3 to shield the gland from infection

Project description:R-spondin (Rspo) signaling is crucial for stem cell renewal and tissue homeostasis in the gastrointestinal tract. In the stomach, Rspo is secreted from myofibroblasts and controls epithelial gland regeneration by inducing proliferation of Wnt-responsive Axin2+ cells in the isthmus of the gland. Infection with H. pylori results in increased expression of stromal Rspo, leading to an expansion of Axin2+ isthmus stem cells and gland hyperplasia. Lgr5+ cells in the gland base are exposed to Rspo3 but the effects of this are not well understood. Here we demonstrate that apart from its activity as a mitogen, endogenous Rspo3 regulates gene expression of Lgr5+ cells in the gastric gland base. Surprisingly, Rspo3 induces differentiation within the Lgr5+ compartment towards secretory deep mucous cells. Moreover, the Rspo3-Lgr5 axis turns out to be a stimulus of epithelial antimicrobial defense. Infection with H. pylori induces a strong antimicrobial response, with Lgr5+ cells expressing antimicrobial compounds that are secreted into the lumen in an Rspo3-dependent manner. Depletion of Lgr5+ cells or knockout of Rspo3 in myofibroblasts leads to hyper-colonization of gastric glands, including the stem cell compartment, whereas systemic application of recombinant Rspo clears H. pylori from the glands. We provide an intriguing, unexpected feature of the Rspo3-Lgr5 axis in the stomach, exhibiting antimicrobial self-protection of the gland to protect the stem cell compartment from invading pathogens.

2019-03-25 | GSE124930 | GEO

RNA-seq of in vitro differentiated human abdominal and gluteal adipocyte cell lines following doxycycline induced RSPO3-knockdown

Project description:GWAS studies and our own work have identified RSPO3 as a gene modulating human body fat distribution. The GWAS signal at RSPO3 is coincident with an eQTL in mature adipocytes. To assess the effects of RSPO3 on abdominal and gluteal adipocyte biology, we undertook inducible RSPO3-knockdown in in vitro differentiated immortalized human abdominal and gluteal adipocyte cell lines (DFAT cells).

2020-06-01 | GSE149294 | GEO

Gene Expression Profiles of 4 CRC PDX models treated by RSPO3 antagonist.

Project description:RSPO is a WNT pathway activator and functions as a potent regulator of stem cell growth in colon. RSPO family members were produced by several human tumors representing multiple tumor types including ovarian, pancreatic, colon, breast and lung cancer. Specific monoclonal antibody antagonists of RSPO family members were developed. In human patient-derived tumor xenograft models, anti-RSPO treatment markedly inhibited tumor growth either as single agents or in combination with chemotherapy. Furthermore, blockade of RSPO signaling reduced the tumorigenicity of cancer cells based on serial transplantation studies. In order to assess the impact of RSPO3 inhibition and gain insight in the anti-RSPO3 treatment mechanism of action, the global gene expression profiles of 4 human colorectal cancer patient derived models (PDX) were performed using Affymetrix microarray for the xenografts treated by the anti-RSPO3 antibody.

2016-03-03 | GSE73906 | GEO

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