Quantitative gene expression in gastrointestinal tissues following consistent activation of ChAT or TH enteric neurons versus non-activated control mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA750149 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Tools to study, and knowledge of, enteric nervous system development and function lag behind brain research. Herein, we deploy recombinant adeno-associated viral (rAAV) vectors with enhanced tropism for the gut to map and activate enteric neurons in mice with spatial and temporal resolution. we employed chemogentics to specifically activate gut neurons that express choline acetyltransferase (ChAT+) or tyrosine hydroxylase (TH+). Targeted activation of ChAT+ or TH+ neuronal populations associated with the gastrointestinal (GI) tract altered the intestinal transcriptome.
2021-08-03 | GSE180961 | GEO
Project description:RERUN OF TH SAMPLES ONLY. Enteric neurons have long been implicated in various physiologies. Recent studies have shown that enteric neurons are affected by the microbiota. However, how certain populations of enteric neurons affect physiology, and methods to ask these questions have been evasive. In this study, we are employing activation DREADDs (designed-receptors exclusively activated by designer drugs) to address the effect of activating subsets of enteric neurons on the host, specifically in the context of the microbiome and metabolome. Two subsets of neurons we are activating are TH (tyrosine-hydroxylase- rate limiting enzyme for catecholamine synthesis) and ChAT (Choline acetyl transferase- rate limiting enzyme for acetylcholine synthesis). Data was acquired using a Thermo Q-Exactive and C18 RP-UHPLC.
2020-02-05 | MSV000084909 | GNPS
Project description:More insights into the character differences between ChAT+ and ChAT- NK cells were obtained based on the gene-expression patterns. A clear delineation between ChAT+ NK cells and ChAT- NK cells was observed, with a total of 300 genes over-expressed and 941 genes under-expressed significantly in the ChAT+ subset. It will provide evidences for further investigation into their functional characters
2017-05-23 | GSE99126 | GEO
Project description:Examination of differentially expressed genes and GSEA analysis of FACS sorted Chat+ and Chat- mature B cells.
2022-03-09 | GSE148863 | GEO
Project description:Purpose: Choline acetyltransferase (ChAT)-expressing epithelial cells are found in the upper and lower airways. In the trachea, they are referred to as brush cells. In the mouse nose two distinct populations of ChAT-eGFP+ cells had been previously described: a population of rare solitary chemosensory cells (SCCs) in the respiratory mucosa and a more abundant population of microvillous cells (MVCs) in the olfactory epithelium. Besides ChAT expression, SCCs share the expression of bitter taste receptors and signaling machinery with tracheal brush cells as well as close association with CGPR+ nerve fibers and an elongated shape. MVCs do not express bitter taste receptors, are not clearly associated with nerves and are smaller in size than SCCs. We have previously reported the transcriptional profile of tracheal ChAT-expressing brush cells but the transcriptional profile of nasal chemosensory ChAT+ epithelial cells has not been reported. Methods: In this study, we isolated nasal ChAT-eGFP+ cells by FACS from naïve ChAT(BAC)-eGFP mice with knockin of eGFP within a BAC spanning the ChAT locus, marking brush cells in the epithelium and performed transcriptome profiling using low input RNA sequencing. We sorted two distinct subsets of ChAT-eGFP+ epithelial cells from the nasal mucosa based on FACS ice and granularity characteristic: ChAT-eGFP+ EpCAM+ FSC/SSChigh (representing 5% of all ChAT-eGFP+ cells) and FSC/SSClow (representing 95% of all ChAT-eGFP+ cells), respectively. We compared them to unfractionated ChAT-eGFP- EpCAM+ epithelial cells. Results: Both nasal ChAT-eGFP subsets shared the core transcriptional profile of chemosensory cells from the intestine, trachea, gallbladder and thymus including the expression of Il25, Pou2f3, Trpm5, Avil, Plcb2 and transcripts of eicosanoid biosynthetic enzymes suggesting that most ChAT-eGFP+ cells in the nose belong to the chemosensory/tuft/brush cel family. The two subsets of nasal ChAT-eGFP+ cells differed in expression of taste receptors and taste receptor signaling machinery. Conclusions: Our study represents the first detailed analysis of the transcriptome of nasal ChAT-eGFP+ cells (brush cells) and identifies two subsets of nasal brush cells that share a core transcriptional signature but differ in expression of bitter taste receptors.
2020-01-16 | GSE139014 | GEO
Project description:The goal of this study was to look at genes that were affected by 69-kDa and/or 82-kDa ChAT proteins in IMR32 cells Experiment Overall Design: The gene expression changes of IMR32 cells stably expressing either 69-kDa or 82-kDa ChAT proteins were anaylzed and compared to control IMR32 wild type cells. 3 biological replicates were anaylzed per condition (69-kDa ChAT expressing cells, 82-kDa ChAT expressing cells, or wild type IMR32 cells) for a total of 9 samples altogether.
2008-06-12 | E-GEOD-3506 | biostudies-arrayexpress
Project description:BACKGROUND Enteric glia contribute to the pathophysiology of various intestinal immune-driven diseases, such as postoperative ileus (POI), a motility disorder and common complication after abdominal surgery. Enteric gliosis of the intestinal muscularis externa (ME) has been identified as part of POI development. However, the glia-restricted responses and activation mechanisms are poorly understood. The sympathetic nervous system becomes rapidly activated by abdominal surgery. It modulates intestinal immunity, innervates all intestinal layers, and directly interfaces with enteric glia. We hypothesized that sympathetic innervation controls enteric glia reactivity in response to surgical trauma. METHODS Sox10iCreERT2/Rpl22HA/+ mice were subjected to a mouse model of laparotomy or intestinal manipulation to induce POI. Histological, protein, and transcriptomic analyses were performed to analyze glia-specific responses. Interactions between the sympathetic nervous system and enteric glia were studied in mice chemically depleted of TH+ sympathetic neurons and glial-restricted Sox10iCreERT2/JellyOPfl/+/Rpl22HA/+ mice, allowing optogenetic stimulation of β-adrenergic downstream signaling and glial-specific transcriptome analyses. A laparotomy model was used to study the effect of sympathetic signaling on enteric glia in the absence of intestinal manipulation. Mechanistic studies included adrenergic receptor expression profiling in vivo and in vitro and adrenergic agonism treatments of primary enteric glial cell cultures to elucidate the role of sympathetic signaling in acute enteric gliosis and POI. RESULTS With ~4000 differentially expressed genes, the most substantial enteric glia response occurs early after intestinal manipulation. During POI, enteric glia switch into a reactive state and continuously shape their microenvironment by releasing inflammatory and migratory factors. Sympathetic denervation reduced the inflammatory response of enteric glia in the early postoperative phase. Optogenetic and pharmacological stimulation of β-adrenergic downstream signaling triggered enteric glia reactivity. Finally, distinct adrenergic agonists revealed β-1/2 adrenoceptors as the molecular targets of sympathetic–driven enteric glial reactivity. CONCLUSIONS Enteric glia act as early responders during post-traumatic intestinal injury and inflammation. Intact sympathetic innervation and active β-adrenergic receptor signaling in enteric glia is a trigger of the immediate glial postoperative inflammatory response. With immune-activating cues originating from the sympathetic nervous system as early as the initial surgical incision, adrenergic signaling in enteric glia presents a promising target for preventing POI development.
2023-11-15 | GSE198889 | GEO
Project description:Using chromatin immunoprecipitation and next-generation sequencing (ChIP-seq), we assessed the effects of acute exposure to oligomeric amyloid-beta on 82-kDa ChAT and SATB1 genome association in human SH-SY5Y neural cells, finding that Aβ-exposure increased 82-kDa ChAT and SATB1 association with gene promoters, introns and matrix attachment regions. We found that both SATB1 and 82-kDa ChAT associate with synapse and cell stress related genes after amyloid-beta exposure.
2016-04-11 | GSE73576 | GEO
Project description:Group 2 innate lymphoid cells (ILC2s) reside in multiple tissues including lymphoid organs and barrier surfaces, and secrete type 2 cytokines including interleukin (IL)-5, IL-9 and IL-13. These cells participate in multiple physiological processes including allergic inflammation, tissue repair, metabolic homeostasis and host defense against helminth infections. Recent studies indicate that neuropeptides can play an important role in regulating ILC2 responses, however, the mechanisms that underlie these processes in vivo remain incompletely defined. Here, we identify that activated ILC2s upregulate choline acetyltransferase (ChAT)—the enzyme responsible for the biosynthesis of acetylcholine (ACh)—following infection with the helminth parasite Nippostrongylus brasiliensis or treatment with alarmins or cytokines including IL-25, IL-33 and thymic stromal lymphopoietin (TSLP). ILC2s also express acetylcholine receptors (AChRs), and ACh administration promotes ILC2 cytokine production and elicits expulsion of helminth infection. In accordance with this, ChAT deficiency in ILC2s leads to defective ILC2 responses and impaired immunity against helminth infection. Together, these results reveal a previously unrecognized role of the ChAT-ACh pathway in promoting type 2 innate immunity to helminth infection.
2021-03-05 | GSE164705 | GEO
Project description:The mouse neuroblastoma N18TG2 clone is unable to differentiate and defective for the enzymes of the biosynthesis of neurotransmitters. The forced expression of choline acetyltransferase (ChAT) in these cells results in the synthesis and release of acetylcholine (Ach) and hence in the expression of neurospecific features and markers. To understand how the expression of ChAT triggered neuronal differentiation, we studied the differences in genome-wide transcription profiles between the N18TG2 parental cells and its ChAT-expressing 2/4 derived clone. The engagement of the 2/4 cells in the neuronal developmental programme was confirmed by the increase of the expression level of several differentiation-related genes and by the reduction of the amount of transcripts of cell-cycle genes. At the same time, we observed a massive reorganisation of cytoskeletal proteins in terms of gene expression, with the accumulation of the nucleoskeletal lamina component Lamin A/C in differentiating cells. The increase of the Lmna transcripts induced by ChAT-espression in 2/4 cells was mimicked treating the parental N18TG2 cells with the acetylcholine-receptor agonist carbachol, thus demonstrating the direct role played by this receptor in neuron nuclei maturation. Conversely, a treatment of 2/4 cells with the muscarinic-receptor antagonist atropine resulted in the reduction of the amount of Lmna RNA. Finally, the hypothesis that Lmna gene product might play a crucial role in the ChAT-dependent molecular differentiation cascade was strongly supported by Lmna knock-down in 2/4 cells leading to the down-regulation of genes involved in differentiation and cytoskeleton formation and to the up-regulation of genes known to regulate self-renewal and stemness. The gene expression profile of the ChAT-expressing 2/4 clone was compared to that of the N18TG2 parental cells, with and without retinoic acid (RA) stimulation using Agilent microarray analysis.
2017-04-18 | E-GEOD-73591 | biostudies-arrayexpress