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Neurotensin regulates proliferation and stem cell function in the small intestine in a nutrient-dependent manner

ABSTRACT: Neurotensin regulates proliferation and stem cell function in the small intestine in a nutrient-dependent manner

PROVIDER: PRJNA758022 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15619232.fastq.gz	Fastqsanger.gz
	SRR15619233.fastq.gz	Fastqsanger.gz
	SRR15619234.fastq.gz	Fastqsanger.gz
	SRR15619235.fastq.gz	Fastqsanger.gz
	SRR15619236.fastq.gz	Fastqsanger.gz

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Neurotensin regulates proliferation and stem cell function in the small intestine in a nutrient-dependent manner

Project description:Background & Aims: Intestinal stem cells (ISCs) are sensitive to dietary alterations and nutrient availability. Neurotensin (NT), a gut peptide localized predominantly to the small bowel and released by fat ingestion, stimulates the growth of intestinal mucosa under basal conditions and during periods of nutrient deprivation, suggesting a possible role for NT on ISC function. Methods: Lgr5-EGFP, NT wild type (Nt+/+) and Lgr5-EGFP, NT knockout (Nt-/-) mice were fed ad libitum (AL) or fasted for 48 h. Small intestine crypts were examined by RNAseq analysis. Results: Loss of NT impaired crypt cell proliferation and ISC function in a manner dependent on nutrient status. Under nutrient-rich conditions, NT stimulated the expression of genes that promote cell cycle progression, leading to crypt cell proliferation. Under conditions of nutrient depletion, NT stimulated WNT/β-catenin signaling and promoted an ISC gene signature, leading to enhanced ISC function. NT was required for the induction of WNT/β-catenin signaling and ISC-specific gene expression during nutrient depletion, and loss of NT reduced crypt cell proliferation and impaired ISC function and Lgr5 expression in the intestine during fasting. Conclusion: Collectively, our findings establish an evolutionarily conserved role for NT in ISC maintenance during nutritional stress.

2021-09-29 | GSE182828 | GEO

Neurotensin Regulates Proliferation and Stem Cell Function in the Small Intestine in a Nutrient-Dependent Manner.

Project description:Background & aimsIntestinal stem cells (ISCs) are sensitive to dietary alterations and nutrient availability. Neurotensin (NT), a gut peptide localized predominantly to the small bowel and released by fat ingestion, stimulates the growth of intestinal mucosa under basal conditions and during periods of nutrient deprivation, suggesting a possible role for NT on ISC function.MethodsLeucine-rich repeat-containing G-protein coupled receptor 5-Enhanced Green Fluorescent Protein (Lgr5-EGFP) NT wild type (Nt+/+) and Lgr5-EGFP NT knockout (Nt-/-) mice were fed ad libitum or fasted for 48 hours. Small intestine tissue and crypts were examined by gene expression analyses, fluorescence-activated cell sorting, Western blot, immunohistochemistry, and crypt-derived organoid culture. Drosophila expressing NT in midgut enteroendocrine cells were fed a standard diet or low-energy diet and esg-green fluorescent protein+ ISCs were quantified via immunofluorescence.ResultsLoss of NT impaired crypt cell proliferation and ISC function in a manner dependent on nutrient status. Under nutrient-rich conditions, NT stimulated extracellular signal-regulated kinases 1 and 2 signaling and the expression of genes that promote cell-cycle progression, leading to crypt cell proliferation. Under conditions of nutrient depletion, NT stimulated WNT/β-catenin signaling and promoted an ISC gene signature, leading to enhanced ISC function. NT was required for the induction of WNT/β-catenin signaling and ISC-specific gene expression during nutrient depletion, and loss of NT reduced crypt cell proliferation and impaired ISC function and Lgr5 expression in the intestine during fasting. Conversely, the expression of NT in midgut enteroendocrine cells of Drosophila prevented loss of ISCs during nutrient depletion.ConclusionsCollectively, our findings establish an evolutionarily conserved role for NT in ISC maintenance during nutritional stress. GSE182828.

| S-EPMC8688554 | biostudies-literature

Unravelling the mechanism of neurotensin recognition by neurotensin receptor 1

Project description:The conformational ensembles of G-protein coupled receptors (GPCRs) include inactive and active states. Spectroscopy techniques, including NMR, show that agonists, antagonists and other ligands shift the ensemble toward specific states depending on the pharmacological efficacy of the ligand. How receptors recognize ligands and the kinetic mechanism underlying this population shift is poorly understood. Here, we investigate the kinetic mechanism of neurotensin recognition by neurotensin receptor 1 (NTS1) using 19F-NMR, hydrogen-deuterium exchange mass spectrometry and stopped-flow fluorescence spectroscopy. Our results indicate slow-exchanging conformational heterogeneity on the extracellular surface of ligand-bound NTS1. Numerical analysis of the kinetic data of neurotensin binding to NTS1 shows that ligand recognition follows an induced fit mechanism, in which conformational changes occur after neurotensin binding. This approach is applicable to other GPCRs to provide insight into the kinetic regulation of ligand recognition by GPCRs.

2023-12-09 | PXD045464 | Pride

The effect of nutrient deprivation on early life small intestine mucosal microbiome and host proteome

Project description:Nutrition has a vital role in shaping the intestinal microbiome. The impact of nutrients and the consequences of enteral deprivation on the small intestinal mucosal microbiota, specifically in early life, has not been well described. Our aim was to study the impact of enteral deprivation on the small intestine mucosal microbiome and to search for factors that shape this interaction in early life. Host seem to be the most dominant factor in the structure of the early life mucosal microbial small intestine community. Under conditions of nutrient deprivation, there are specific changes in host proteomics. Further research is needed to better define and understand this host-microbe-nutrition interaction in the small intestine.

2024-07-16 | PXD044961 | Pride

Neurotensin-Neurotensin Receptor 2 signaling in adipocytes regulates food intake through ceramide metabolism

Project description:Neurotensin-Neurotensin Receptor 2 signaling in adipocytes regulates food intake through ceramide metabolism

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Regionally defined stem cell growth directs cell fate during intestinal nutrient adaptation

Project description:The adult intestine is a regionalized organ, whose size and cellular composition is adjusted in response to nutrient status. This involves dynamic regulation of intestinal stem cell (ISC) proliferation and differentiation. How nutrient signaling integrates with mechanisms controlling cell fate to achieve regional changes in intestinal cell composition remains unclear. Here we show that nutrient adaptation involves highly region-specific control of intestinal cell size, number and differentiation. Our data uncovered a mechanism by which mTOR complex 1 activation increases ISC size in a region-specific manner. This promotes Delta expression to direct cell fate towards the absorptive enteroblast lineage, while inhibiting secretory enteroendocrine cell differentiation. Thus, ISC size acts as an early fate determinant allowing regional control of intestinal cell differentiation in response to nutrition.

2024-02-14 | GSE222254 | GEO

Molecular profiling of lateral septum neurotensin neurons using viralTRAP

Project description:The lateral septum contains a number of molecularly defined cell populations. We used the viral-TRAP protocol (Nectow et al.,2017) to profile lateral septum neurotensin neurons.

2020-08-30 | GSE154758 | GEO

Nutrient-derived signals regulate eosinophil adaptation to the small intestine

Project description:Nutrient-derived signals regulate eosinophil adaptation to the small intestine

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eIF4GI Links Nutrient Sensing by mTOR to Cell Proliferation and Inhibition of Autophagy

Project description:Translation initiation factors have complex functions in cells which are not yet understood. We show that depletion of initiation factor eIF4GI only modestly reduces overall protein synthesis in cells, but phenocopies nutrient-starvation or inhibition of protein kinase mTOR, a key nutrient sensor. eIF4GI depletion impairs cell proliferation, bioenergetics and mitochondrial activity, thereby promoting autophagy. Translation of mRNAs involved in cell growth, proliferation and bioenergetics were selectively inhibited by reduction of eIF4GI, whereas mRNAs encoding proliferation inhibitors and catabolic pathway factors were increased. Depletion or over-expression of other eIF4G family members did not recapitulate these results. The majority of mRNAs that were translationally impaired with eIF4GI depletion were excluded from polyribosomes due to the presence of multiple upstream open reading frames and low mRNA abundance. These results suggest that the high levels of eIF4GI observed in many breast cancers might act to specifically increase proliferation, prevent autophagy and release tumor cells from control by nutrient sensing. Global regulation of transcription and polysomal association in eIF4GI-silenced cells. Keywords: Gene Silencing

2008-04-01 | GSE11011 | GEO

Single-cell transcriptome analysis reveals differential nutrient absorption functions in human intestine

Project description:Single-cell transcriptome analysis reveals differential nutrient absorption functions in human intestine

| PRJNA518129 | ENA