Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of adult zebrafish enteric nervous system

ABSTRACT: The enteric nervous system (ENS) encompasses the intrinsic neuroglia networks of the gastrointestinal (GI) tract that are essential for digestive function and gut homeostasis. To investigate the ENS of zebrafish, we carried out bulk RNA sequencing on nuclei purified by FACS (fluorescent-activated cell sorting) representing both the Cherry+ (ENS) and Cherry- (non-ENS) muscularis externa cell populations of Tg(sox10:Cre;Cherry) zebrafish gut.

ORGANISM(S): Danio rerio

PROVIDER: GSE145885 | GEO | 2020/09/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Neuro-immune Crosstalk in the Enteric Nervous System from Early Postnatal Development to Adulthood

Project description:Single-cell RNA sequencing using SmartSEQ2 platform of Cx3cr1+ macrophages isolated from the muscularis externa of mice of 10 and of 56 days of age.

2023-04-16 | E-MTAB-11453 | biostudies-arrayexpress

Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections

Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.

2021-08-17 | GSE182294 | GEO

Spatiotemporal dynamics of the developing zebrafish enteric nervous system at the whole organ level

Project description:Neural crest cells give rise to the neurons of the enteric nervous system (ENS) that innervate the gastrointestinal tract to regulate gut motility. The immense size and distinct subregions of the gut present a challenge to understanding the spatial organization and sequential differentiation of different neuronal subtypes. Here, we profile enteric neurons and progenitors at single cell resolution during zebrafish embryonic and larval development to provide a near complete picture of transcriptional changes that accompany emergence of ENS neurons throughout the gastrointestinal tract. Multiplex spatial RNA transcript analysis reveals the temporal order and distinct localization patterns of neuronal subtypes along the length of the gut. Finally, we show that functional perturbation of select transcription factors Ebf1a, Gata3 and Satb2 alters the cell fate choice, respectively, of inhibitory, excitatory and serotonergic neuronal subtypes in the developing ENS.

2024-08-30 | GSE274407 | GEO

Gene expression analysis following neurogenesis of adult enteric glia/progenitor cells

Project description:Enteric glia cells (EGCs) are highly plastic and has been shown to give rise to neurons in adult gut upon injury to the enteric nervous system (ENS). To better characterise the dynamic molecular changes associated with EGC activation and its subsequent neurogenic differentation trajectory, we performed bulk RNAseq experiments from FACS sorted lineage-labelled cells (Sox10::CreERT2;R26-tdTomato) from adult small intestines (DIV0) and compared their transcriptomic profiles to cultured FACS sorted tdTomato+ cells from days in vitro (DIV) 4, 11 and 20, which were subjected to a protocol to support neurogenesis in culture.

2023-07-26 | GSE160196 | GEO

Bulk RNA-sequencing of self-maintaining versus monocyte-replaced gut macrophages

Project description:Self-maintaining gMacs are present in the submucosal and myenteric plexus of the intestine where they maintain enteric neurons and submucosal vasculature YFP-positive and YFP-negative CD11b+, CD64+ macrophages were sorted from lamina propria and muscularis externa of Cx3cr1CreERT2.Rosa26-LSL-YFP animals, 35 weeks after tamoxifen administration. Four biological replicates each. YFP-positive and YFP-negative were compared within lamina propria and muscularis externa

2018-07-30 | E-MTAB-6977 | biostudies-arrayexpress

Sequencing Reveals miRNAs Enriched in the Developing Mouse Enteric Nervous System [miRNA]

Project description:The enteric nervous system (ENS) is an essential network of neurons and glia in the bowel wall. Defects in ENS development can result in Hirschsprung disease (HSCR), a life-threatening condition characterized by severe constipation, abdominal distention, bilious vomiting, and failure to thrive. A growing body of literature connects HSCR to alterations in miRNA expression, but there are limited data on the normal miRNA landscape in the developing ENS. We sequenced small RNAs (smRNA-seq) and messenger RNAs (mRNA-seq) in ENS precursors of mid-gestation Ednrb-EGFP mice and compared them to aggregated RNA from all other cells in the developing bowel. Our smRNA-seq results identified 73 miRNAs that were significantly enriched and highly expressed in the developing ENS, with miR-9, miR-27b, miR-124, miR-137, and miR-488 as our top 5 miRNAs that are conserved in humans. However, contrary to prior reports, our follow-up analyses of miR-137 showed that loss of Mir137 in Nestin-cre, Wnt1-cre, Sox10-cre, or Baf53b-cre lineage cells had no effect on mouse survival or ENS development. Our data provide important context for future studies of miRNA in HSCR and other ENS diseases and highlight open questions about facility-specific factors in development.

2023-12-26 | GSE250527 | GEO

Sequencing Reveals miRNAs Enriched in the Developing Mouse Enteric Nervous System [mRNA]

2023-12-26 | GSE250526 | GEO

Vancomycin Induced Gut Microbial Dysbiosis Alters Enteric Neuron-Macrophage Interactions During a Critical Period of Postnatal Development

Project description:Vancomycin is a broad-spectrum antibiotic widely used in cases of suspected sepsis in premature neonates. While appropriate and potentially lifesaving in this setting, early life antibiotic exposure alters the developing microbiome and is associated with increased risk of deadly complications, including late-onset sepsis (LOS) and necrotizing enterocolitis (NEC). Recent studies show that neonatal vancomycin treatment disrupts postnatal enteric nervous system (ENS) development in mouse pups, which is in part dependent upon neuro-immune interactions. This suggests that early life antibiotic exposure could disrupt these interactions in the neonatal gut. Notably, a subset of tissue-resident intestinal macrophages, muscularis macrophages, have been identified as important contributors to the development of the postnatal ENS. We hypothesized that vancomycin-induced neonatal dysbiosis impacts postnatal ENS development through effects on macrophages. Using a mouse model, we found that exposure to vancomycin in the first ten days of life, but not in adult mice, resulted in an expansion of pro-inflammatory colonic macrophages by increasing the recruitment of bone-marrow derived macrophages. Single cell RNA sequencing of neonatal colonic macrophages revealed that early-life vancomycin exposure was associated with an increase in immature and inflammatory macrophages, consistent with an influx of circulating monocytes differentiating into macrophages. Lineage tracing confirmed that vancomycin significantly increased non-yolk sac derived macrophage population. Consistent with these results, early life vancomycin exposure did not expand the colonic macrophage population nor decrease enteric neuron density in CCR2 deficient mice. Collectively, these findings demonstrate that early life vancomycin exposure alters macrophage number and phenotypes in distinct ways compared to vancomycin exposure in adult mice and results in altered ENS development.

2023-11-13 | GSE245019 | GEO

Gene expression profile at single cell level of the enteric nervous system (ENS) of 5 days post fertilization (dpf) zebrafish

Project description:We used single cell RNA sequencing (scRNA-seq) to characterize the ENS in the zebrafish intestine.

2023-05-31 | GSE225510 | GEO

Loss of enteric neuronal Ndrg4 promotes colorectal cancer via increased release of Nid1 and Fbln2

Project description:The N-Myc Downstream-Regulated Gene 4 (NDRG4), a prominent biomarker for colorectal cancer (CRC), is specifically expressed by enteric neurons. Considering that nerves are important members of the tumor microenvironment, we here establish different Ndrg4 knockout (Ndrg4-/-) CRC models and an in-direct co-culture of primary enteric nervous system (ENS) cells and intestinal organoids to identify whether the ENS, via NDRG4, affects intestinal tumorigenesis. Linking immunostainings and gastrointestinal motility (GI) assays, we show that absence of Ndrg4 does not trigger any functional or morphological GI-abnormalities. However, combining in vivo, in vitro and quantitative proteomics data, we uncover that Ndrg4 knockdown is associated with enlarged intestinal adenoma development and that organoid growth is boosted by the Ndrg4-/- ENS cell secretome, which is enriched for Nidogen-1 (Nid1) and Fibulin-2 (Fbln2). Moreover, NID1 and FBLN2 are expressed in enteric neurons, enhance tumorigenic capacities of CRC cells and are enriched in human CRC secretomes. Hence, we provide evidence that the ENS, via loss of Ndrg4, is involved in colorectal pathogenesis and that ENS-derived Nidogen-1 and Fibulin-2 enhance colorectal carcinogenesis.

2021-04-23 | PXD024502 | Pride

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