Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells (small intestinal epithelium)

ABSTRACT: Crypt cells (mainly stem and transit amplifying (TA) cells) in Adipfl/flpVilli-CreT (gut epithelial cell adiponectin conditioned knockout) mice exhibited stronger ability of renewal and differentiation. ScRNA-seq found that there had much more enrichment intestinal stem and TA cells in Adipfl/flpVilli-CreT mice. The renewal and development of gut epithelial cells in irradiated or DSS (dextran sulfate sodium) treated Adipfl/flpVilli-CreT mice was faster than control Adipfl/flp mice. In vitro culture gut organoid of Adipfl/flpVilli-CreT mice exhibited faster growth than those from Adipfl/flp mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE270099 | GEO | 2024/06/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells

Project description:We here demonstrate that adiponectin in Paneth cells can suppress renewal and differentiation of gut stem cells through adiponectin receptor 1 (AdipR1). Crypt cells (mainly stem and transit amplifying (TA) cells) in Adipfl/flpVilli-CreT (gut epithelial cell adiponectin conditioned knockout) mice exhibited stronger ability of renewal and differentiation. ScRNA-seq found that there had much more enrichment intestinal stem and TA cells in Adipfl/flpVilli-CreT mice. The renewal and development of gut epithelial cells in irradiated or DSS (dextran sulfate sodium) treated Adipfl/flpVilli-CreT mice was faster than control Adipfl/flp mice. In vitro culture gut organoid of Adipfl/flpVilli-CreT mice exhibited faster growth than those from Adipfl/flp mice. The gut epithelial cells in AdipR1 knockout (KO) mice had much longer crypts than control mice. Interestingly, indole-3-acetic acid (IAA) from gut microbiota could control the expression of adiponectin to promote the renewal and proliferation of gut stem cells. In vitro culture organoid also showed faster development after exposing to IAA. Thus, adiponectin, which is regulated by gut microbiota derived IAA controls the renewal and differentiation of gut stem cells to maintain the homeostasis of epithelial cells.

2024-06-14 | GSE269692 | GEO

Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells

Project description:Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells

| PRJNA1123244 | ENA

Single cell RNA sequencing analysis of germ free (GF) mouse Paneth cells and microbiome-transferred exGF mouse Paneth cells.

Project description:The single cell level Paneth cell transcriptome under gnotobiotic condition has not been resolved. How gut microbiome modulates Paneth cell transcriptome at single cell level in germ-free mice was not known. We used a flow cytometry method to isolate highly pure ileal Paneth cells from germ free (GF) Paneth cell reporter mice (Lyz1-3'UTR-IRES-CreER) and from exGF Paneth cell reporter mice that were transplanted with wild type C57B/l6 mouse gut microbiota (exGF+B6M). These isolated Paneth cells were subjected to single cell RNA sequencing by 10xGenomics.

2023-09-01 | GSE237328 | GEO

Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells (small intestinal epithelium)

Project description:Adiponectin regulated by IAA in Paneth cells controls renewal and differentiation of gut stem cells to maintain homeostasis of epithelial cells (small intestinal epithelium)

| PRJNA1124989 | ENA

Adiponectin inhibits acquisition of the Lyme disease agent by ticks [Tick]

Project description:Tick gut and salivary gland global gene expression change after feeding on adiponectin wildtype and knockout mice

2024-05-01 | GSE233660 | GEO

Colonic Gene expression in mice colonized with human gut microbiota from healthy and IBS patients

Project description:Irritable Bowel Syndrome (IBS) is a disorder of the gut-brain axis, characterized by altered gut function and frequent psychiatric co-morbidity. Although altered intestinal microbiome profiles have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role of the microbiota, we colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with accompanying anxiety, and monitored gut function and behavior. Mouse microbiota profiles clustered according to their human donors. Despite having taxonomically similar composition as controls, mice with IBS microbiota had distinct serum metabolomic profiles related to neuro- and immunomodulation. Mice with IBS, but not control microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation and anxiety-like behavior. These results support the notion that the microbiota contributes to both intestinal and behavioral manifestations of IBS and rationalize the use of microbiota-directed therapies in ameliorating IBS.

2017-03-02 | GSE61841 | GEO

Integrin αEβ7+ T cells direct intestinal stem cell fate decision via adhesive signaling

Project description:Intestinal stem cells (ISCs) maintain gut homeostasis by differentiating into different epithelial cell types, which is precisely regulated by a niche of accessory cell types. In the niche, lymphocytes may interact with stem and transient amplifying (TA) cells in the intestinal crypts. However, it is unknown whether and how the lymphocyte- stem/TA cell contacts affect ISC differentiation. Here we discover and mechanistically dissect the role of T cell-stem/TA cell contacts in ISC fate decision. We found T cells are often seen in contact with ISCs and TA cells in the small intestinal crypts, whereas B cell-stem/TA cell interaction was hardly observed. Using single-cell RNA sequencing and immunostaining, we showed that depletion of intestinal lymphocytes resulted in aberrant ISC differentiation in mice, with decreased Paneth and goblet cells, increased enteroendocrine cells and impaired enterocyte maturation. Transferring T cells but not B cells into those mice efficiently restored normal ISC differentiation. Mechanistically, integrin αEβ7 on T cells binds to E-cadherin on ISCs and TA cells. Blocking this adhesion suppressed Wnt signaling in ISCs and TA cells and promoted Notch signaling in TA cells, leading to defective ISC differentiation. In vitro study using purified αEβ7 protein showed consistent effects on the intestinal organoid differentiation. Taken together, our study reveals that the gut-resident integrin αEb7+ T cells regulate the ISC differentiation through adhesion between αEβ7 on T cells and E-cadherin on ISCs and TA cells. The αEβ7-E-cadherin adhesive signaling is critical for the fate decision of ISCs and the maintenance of intestinal homeostasis.

2022-08-02 | GSE135316 | GEO

Expression of FABP4, adipsin and adiponectin in Paneth cells is modulated by gut Lactobacillus.

Project description:We here found that intestinal epithelial Paneth cells secrete FABP4, adipsin and adiponectin in both mice and human. Deletion of Paneth cell results in the decrease of FABP4, adipsin and adiponectin not only in intestinal crypt cells but also in sera, suggesting that they may influence the state of the whole body. We also demonstrate that expression of FABP4, adipsin and adiponectin may be modulated by specific gut microbiota. In germ-free (GF) mice, the expression of FABP4, adipsin and adiponectin were lower or difficult to be detected. Feces transplantation promoted the expression of FABP4, adipsin and adiponectin in gut epithelial Paneth cells. We have found that Lactobacillus NK6 colony, which has the highest similarity with Lactobacillus taiwanensis strain BCRC 17755, may induce the expression of FABP4, adipsin and adiponectin through TRAF2 and TRAF6 ubiquitination mediated NF-?B signaling. Taken together, our findings set up a novel mechanism for FABP4, adipsin and adiponectin through gut microbiota mediating expression in gut Paneth cells.

| S-EPMC4685643 | biostudies-literature

CDC42 controlled apical-basal polarity regulates intestinal stem cell to transit amplifying cell fate transition via YAP-EGF-mTOR signaling

Project description:Epithelial polarity is controlled by a polarity machinery including the Rho GTPase CDC42 and Scribble/PAR. By using intestinal stem cell (ISC)-specific deletion of CDC42 in Olfm4-IRES-eGFPCreERT2;CDC42flox/flox mice, we found that ISC-initiated CDC42 loss caused a drastic hyper-proliferation of transit amplifying (TA) cells and disrupted epithelial polarity. CDC42-null crypts displayed expanded TA cell and diminished ISC populations, accompanied by elevated hippo signaling via YAP/TAZ - Ereg and mTOR activation, independent from canonical Wnt signaling. YAP/TAZ conditional knockout restored the balance of ISC/TA cell populations and crypt proliferation but did not rescue the polarity in CDC42-null small intestine. mTOR or EGFR inhibitor treatment of CDC42 KO mice exhibited similar rescuing effects without affecting YAP/TAZ signaling. Inducible ablation of Scribble in intestinal epithelial cells mimics that of CDC42 KO defects including crypt hyperplasia and hippo signaling activation. Mammalian epithelial polarity regulates ISC and TA cell fate and proliferation via a hippo-Ereg-mTOR cascade.

2021-10-23 | GSE166736 | GEO

Intestinal Paneth cell differentiation relies on asymmetric regulation of Wnt signaling by Daam1/2

Project description:Purification of RNF43 interactors was performed with the following 4 different constructs: (i) empty vector (EV) as a control for background contaminants/non-specific protein binding; (ii) full-length RNF43 protein (RNF43 FL); (iii) deleted version of RNF43 harboring only the PA-TA domain (RNF43 Δ1); and (iv) deleted version of RNF43 harboring only the PA-TA-RING domain (RNF43 Δ3). HEK293T cells were transfected with pcDNA3-FLAG-HA- RNF43 (FL, Δ1 or Δ3).

2023-10-19 | PXD043151 | JPOST Repository

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data