Similar Datasets
Project description:Co-cultures of enteric neurons and T cells
| PRJNA691242 | ENA
Project description:We reported transcriptional characterization of enteric neurons with the stimulations of C.ramosum or P.magnus in Germ-free colons
2021-02-18 | GSE164575 | GEO
Project description:Enteric nervous system is involved in the regulation of intestinal inflammation. We developped mouse primary cultures of enteric nervous system to study impact of LPS, as pro-inflammatory mediator, and of the pro-drug 6-mercaptopurine on enteric inflammatory pathways We used microarrays to detail the global programme of gene expression underlying enteric neuro-inflammation and identified classes of up-regulated genes during this process.
2021-04-02 | GSE171308 | GEO
Project description:Profiling of transcriptional changes in rat astrocytes when co-cultured with neurons: comparison of astrocytes cultured alone with astrocytes co-cultured with mouse hippocampal neurons. Co-cultured astrocytes are isolated using cold jet, a novel tool for these neuron-glia cultures. Over the last decade, the importance of astrocyte-neuron communication in neuronal development and synaptic plasticity has become increasingly clear. Since neuron-astrocyte interactions represent highly dynamic and reciprocal processes, we hypothesized that at least part of the involved astrocyte genes may be regulated as a consequence of their interactions with maturing neurons. In order to identify such neuron-induced astrocyte genes in vitro, we tested the effectiveness of the ‘cold jet’, a new method for separation of neurons from co-cultured astrocytes. The cold jet method is performed under ice-cold conditions and avoids protease-mediated isolation of astrocytes or time-consuming centrifugation, yielding intact astrocyte mRNA with approximately 90% of neuronal RNA removed. Using this method, we executed genome-wide profiling in which RNA derived from astrocyte-only cultures was compared with astrocyte RNA derived from differentiating neuron-astrocyte co-cultures. Data analysis revealed changes in expression of a large number of mRNAs and biological processes, including novel findings. Thus, cold jet is an efficient method to separate astrocytes from neurons in co-culture, and in this study reveals that neurons induce robust gene-expression changes in co-cultured astrocytes.
2016-11-09 | GSE52481 | GEO
Project description:Microbial density and diversity increase in distal intestinal segments, affecting tissue physiology, metabolism, and function of both the immune and nervous systems. We characterized the influence of the microbiota on murine intrinsic enteric-associated neurons (iEAN). We found that iEAN are functionally adapted to the intestinal segment they occupy, with a stronger microbiota influence on ileal and colonic neurons. Chemogenetic characterization of microbiota-influenced iEAN identified a subset of viscerofugal CART+ neurons, enriched in the ileum and colon, able to modulate feeding and glucose metabolism. Retro- and anterograde tracing revealed that CART+ viscerofugal neurons send axons to the prevertebral ganglia and are poly-synaptically connected to the liver and pancreas. Microbiota depletion led to NLRP6 and Caspase 11-dependent loss of CART+ neurons, and impaired liver-mediated gluconeogenesis. Our results demonstrate a region-specific adaptation of enteric neurons and indicate that iEAN subsets are capable of regulating blood glucose levels independently from the central nervous system.
2020-08-13 | GSE156142 | GEO
Project description:Epigenetic regulatory mechanisms are underappreciated but critical for enteric nervous system (ENS) development and maintenance. We discovered that fetal loss of the epigenetic regulator Bap1 in the ENS lineage causes severe postnatal bowel dysfunction and early death in Tyrosinase-Cre; Bap1fl/fl mice. Bap1-depleted ENS appears normal in neonates, however, by postnatal day 15 (P15), Bap1-deficient enteric neurons are largely absent from the small and large intestine of Tyrosinase-Cre; Bap1fl/fl mice. Bowel motility becomes markedly abnormal with disproportionate loss of cholinergic neurons. Single-cell RNA sequencing at P5 shows that fetal Bap1 loss inTyrosinase-Cre; Bap1fl/fl mice markedly alters the composition and relative proportions of enteric neuron subtypes. In contrast, postnatal deletion of Bap1 did not cause enteric neuron loss or impaired bowel motility. These findings suggest that BAP1 is critical for postnatal enteric neuron differentiation and for enteric neuron survival.
2024-04-01 | GSE242001 | GEO
Project description:Bowel function requires coordinated activity of many enteric neuron subtypes. Clear definition of subtype-specific gene expression may facilitate molecular diagnoses for bowel motility disorders. Using adult mouse colon RNAseq data from 635 myenteric neurons and 707 E17.5 neurons, we defined seven adult myenteric neuron subtypes, eight E17.5 neuron subtypes and hundreds of differentially-expressed genes. Manually dissected human colon myenteric plexus yielded data from 48 neurons, 3798 glia, 5568 smooth muscle, 377 interstitial cells, and 2153 macrophages. Immunohistochemistry demonstrated differential protein abundance for BNC2, PBX3, RBFOX1, TBX2, and TBX3 in enteric neuron subtypes. Conditional Tbx3 loss reduced NOS1-expressing myenteric neurons. Differential Gfra1 and Gfra2 expression coupled with calcium imaging revealed that GDNF and neurturin acutely and differentially regulate activity of ~50% of myenteric neurons with distinct effects on smooth muscle contractions. This insight into enteric nervous system biology provides a foundation for future studies of bowel motility disorders.
2021-01-01 | GSE156905 | GEO
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:Resting and proliferating Treg cells from NOD mice G-BMDC-Treg co-cultures were sorted out and anlyzed for differential gene expresion pattern. Proliferating Treg cells had increased expression of )X40, Notch and IL-2R related genes inaddition to Foxp3 and its functional partners genes.
2016-05-04 | GSE81051 | GEO
Project description:Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays. To generate Tregs and Tconvs in multiple states of activation, naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs were sorted from blood of 7 healthy adults and RNA was isolated ex vivo or after stimulation for 40h, promoting activation-induced FOXP3 in Tconvs. The gene-expression profile of the eight cell subsets was analyzed. 7 adult healthy control samples were sorted into 4 subsets: naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs. These were used for RNA ex vivo and after 40h stimulation with anti-CD3/CD28 beads to induce an activation phenotype.
2016-01-19 | E-GEOD-76598 | biostudies-arrayexpress