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Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation

ABSTRACT: Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation

PROVIDER: PRJNA1238249 | ENA |

REPOSITORIES: ENA

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	SRR32778084.fastq.gz	Fastqsanger.gz

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Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation

Project description:In this study, we investigated the involvement of formyl peptide receptor 2 (FPR2) in intestinal epithelium homeostasis and the underlying mechanisms by comparing the transcriptome profiles of intestinal crypts from intestinal epithelial-specific knockout (Fpr2VKO) and control (Fpr2f/f) mice.

2025-03-24 | GSE292366 | GEO

Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation [scRNA-seq]

Project description:To investigate the contribution of formyl peptide receptor 2 (FPR2) to intestinal epithelium homeostasis and the underlying mechanisms, we isolated small intestinal crypts from intestinal epithelial-specific knockout (Fpr2VKO) and control (Fpr2f/f) mice, isolated epithelial cells from the crypts and performed single-cell RNA sequencing (scRNA-Seq). The transcriptome profiles of Fpr2VKO and Fpr2f/f mice were compared.

2025-03-31 | GSE292802 | GEO

Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation [scRNA-seq]

Project description:Formyl peptide receptor 2 contributes to intestinal epithelium homeostasis by regulating intestinal stem cell proliferation and differentiation [scRNA-seq]

| PRJNA1241283 | ENA

Type I Interferons Control Proliferation and Function of Intestinal Epithelium

Project description:Wnt pathway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prevent development of cancer and barrier dysfunction. Although type 1 interferons (IFN) produced in the gut under influence of microbiota are known for their anti-proliferative effects, the role of these cytokines in regulating intestinal epithelial renewal is largely unknown. Here we report a novel role for IFN in the context of intestinal knockout of casein kinase 1Î± (CK1Î±), which controls ubiquitination and degradation of both Î²-catenin and the IFNAR1 chain of the IFN receptor. Ablation of CK1Î± leads to activation of both Î²-catenin and IFN pathway and prevents unlimited proliferation of intestinal epithelial cells despite constitutive Î²-catenin activity. IFN signaling contributes to activation of the p53 pathway and appearance of apoptotic and senescence markers in the CK1Î±-deficient gut. Concurrent genetic ablation of CK1Î± and IFNAR1 leads to intestinal hyperplasia, robust attenuation of apoptosis, and rapid and lethal loss of the barrier function. These data indicate that IFN plays an important role in controlling proliferation and function of intestinal epithelium in the context of Î²-catenin activation. Two conditions were examined, with 2 replicates for each condition, yielding 4 samples in total.

2016-01-05 | E-GEOD-76512 | biostudies-arrayexpress

Type I Interferons Control Proliferation and Function of Intestinal Epithelium

Project description:Wnt pathway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prevent development of cancer and barrier dysfunction. Although type 1 interferons (IFN) produced in the gut under influence of microbiota are known for their anti-proliferative effects, the role of these cytokines in regulating intestinal epithelial renewal is largely unknown. Here we report a novel role for IFN in the context of intestinal knockout of casein kinase 1α (CK1α), which controls ubiquitination and degradation of both β-catenin and the IFNAR1 chain of the IFN receptor. Ablation of CK1α leads to activation of both β-catenin and IFN pathway and prevents unlimited proliferation of intestinal epithelial cells despite constitutive β-catenin activity. IFN signaling contributes to activation of the p53 pathway and appearance of apoptotic and senescence markers in the CK1α-deficient gut. Concurrent genetic ablation of CK1α and IFNAR1 leads to intestinal hyperplasia, robust attenuation of apoptosis, and rapid and lethal loss of the barrier function. These data indicate that IFN plays an important role in controlling proliferation and function of intestinal epithelium in the context of β-catenin activation.

2016-01-05 | GSE76512 | GEO

Semaglutide attenuates obesity-induced impact on intestinal epithelium

Project description:Obesity, a complex ailment, has demonstrated promising weight reduction outcomes with glucagon-like peptide-1 receptor agonists (GLP-1RA) drugs like semaglutide. Nevertheless, their intricate mechanisms remain elusive. In this study, we constructed single-cell transcriptomic profiles of intestinal epithelium from individuals with normal and high BMI, revealing significant transcriptomic and metabolic alterations.

2025-03-03 | GSE261178 | GEO

ATAC-sequencing mice small intestinal epithelium with intestinal epithelium specific LSD1 knock out compared to wild type

Project description:To study the epigenetic regulation of intestinal epithelium we focus on the role of chromatin modulators. Lysine-specific histone demethylase 1a (KDM1A, LSD1) is one of the enzymes that can erase the H3K4me1/2 mark. To assess the role of LSD1 in intestinal epithelium we studied wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We found that KO mice completely lack Paneth cells, and have altered stem cell characteristics compared to WT littermates. To assess genome-wide ATAC levels in WT and KO small intestines, we isolated intestinal epithelium tissue from wild type mice and LSD1 KO mice. This tissue was digested to single cells and performed ATAC seq as described in the protocols.

2021-03-23 | E-MTAB-8718 | biostudies-arrayexpress

Gall&Pin2022 - ODE model of the intestinal epithelium

Project description:We developed a compartmental model of the small intestinal epithelium that describes stem and progenitor cell proliferation and differentiation and cell migration onto the villus. The model includes a negative feedback loop from villus cells to regulate crypt proliferation and integrates heterogeneous epithelial-related processes, such as the transcriptional profile, citrulline kinetics and probability of diarrhea.

2023-09-04 | MODEL2212120003 | BioModels

Spatial discordances between mRNAs and proteins in the intestinal epithelium

Project description:We obtained a spatial measurement of RNA and Proteins in the small intestinal epithelium along the crypt-villus axis. We found that both were spatially heterogeneous, yet often spatially anti-correlated. We developed a Bayesian approach to infer protein translation and degradation rates from the combined spatial profiles, and demonstrate that space-independent protein-synthesis delays can explain the mRNA-protein discordances. Our work provides a proteomic spatial blueprint of the Intestinal epithelium and highlights the importance of protein measurements for inferring states of tissue cells that operate outside of steady state

2021-11-02 | PXD024906 | Pride

Sox4 regulates proliferation, differentiation, and DNA methylation patterns in the intestinal epithelium

Project description:Intestinal stem cells (ISCs) are responsible for maintaining the physiological function of the intestinal epithelium through the production of differentiated absorptive and secretory cellular lineages. In addition to producing specialized functional cells, ISCs must also drive constant proliferation in order to maintain the especially high rate of cellular turnover in the intestinal epithelium, which undergoes near total renewal every 5-7 days. Understanding the transcriptional mechanisms that control how ISCs and transit-amplifying progenitors (TAs) balance differentiation and proliferation in the intestine may provide valuable insight into common pathologies, such as inflammatory bowel disease and cancer. Here, we show that the Sry¬¬-box containing transcription factor, Sox4, is involved in the regulation of proliferation in the ISC/TA zone, the expression of ISC-associated genes, and the differentiation of enteroendocrine (EE) cells. Interestingly, we also observed a significant reduction in the expression of the methylcytosine dioxygenase, Tet1, in Sox4-deficient intestines. We find that Tet1, which initiates derepression of target genes via DNA demethylation, is specifically upregulated in ISC populations in wild-type animals. Additionally, Sox4-deficient intestines showed a significant reduction in levels of 5-hydroxymethylcytosine, the catalytic byproduct of TET protein activity, in the ISC/TA zone. Together, our data demonstrate that Sox4 regulates differentiation and proliferation in the intestinal epithelium, and suggests that it may influence these processes through induction of Tet1 and subsequent derepression of target genes through epigenetic mechanisms.

2014-12-31 | GSE52675 | GEO

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