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RNA sequencing of norepinephrine- or vehicle-treated mouse colon cancer organoids

ABSTRACT: To profile transcriptomic alterations induced by catecholamine stimulation, we treated ApcΔ/Δ, KrasG12D/Δ, Trp53Δ/Δ mouse colon cancer organoids with norepinephrine or vehicle and then performed RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE243326 | GEO | 2024/07/30

REPOSITORIES: GEO

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RNA sequencing of bethanechol- or vehicle-treated mouse colon cancer organoids

Project description:To profile transcriptomic alterations induced by muscarinic receptor stimulation, we treated ApcΔ/Δ, KrasG12D/Δ, Trp53Δ/Δ mouse colon cancer organoids with bethanechol or vehicle and then performed RNA sequencing.

2026-05-21 | GSE309316 | GEO

RNA sequencing of norepinephrine- or vehicle-treated mouse colon cancer organoids

Project description:RNA sequencing of norepinephrine- or vehicle-treated mouse colon cancer organoids

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Differential gene expression in ovarian cancer cell lines treated with vehicle or norepinephrine

2011-12-14 | GSE34405 | GEO

Differential gene expression in ovarian cancer cell lines treated with vehicle or norepinephrine

Project description:Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine. The primary research question is whether ovarian cancer cell gene expression differs as a function of norepinephrine exposure. Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine.

2011-12-14 | E-GEOD-34405 | biostudies-arrayexpress

Effect of norepinephrine and UK 14,304 treatment on murine small intestinal organoids

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2023-05-09 | GSE230088 | GEO

Changes in tRNA wobble modifications under a norepinephrine gradient coincide with codon-biased translation and induction of virulence in EHEC O157:H7

Project description:The goal of this study was to investigate how Enterohemorrhagic Escherichia coli O157:H7 (EHEC) strain EDL933 remodels its tRNA pool in response to the catecholamine hormone norepinephrine, a host-derived cue that stimulates virulence in this pathogen. Here, we performed Absolute Quantitative RNA-sequencing (AQRNA-seq) to measure levels of tRNA isoacceptors in EHEC samples exposed to 0, 25, and 50 micromolar norepinephrine.

2026-04-17 | GSE309283 | GEO

scRNA-seq of mouse colon after THC administration

Project description:We studied the effects of delta-9-tetrhydrocannabinol (THC) on mouse colon cells, 24 hours after a single administration of THC (10mg/kg) or Vehicle (VEH) control.

2020-08-05 | GSE155669 | GEO

RNAseq of Islets Isolated from Near Term Fetal Sheep after 7-day Infusion of Norepinephrine or Vehicle Control

Project description:The study objective was to determine differentially expressed mRNA transcripts in pancreatic islets from fetal sheep exposed to persistent elevations in stress hormone norepinephrine to isolate effects of chronic adrenergic signaling on fetal islets. Ultimately, these data can be compared to islets from fetuses with placental insufficiency-induced intrauterine growth restriction, where there is known increases in norepinephrine.

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Norepinephrine transporter-deficient neural crest cells

Project description:Background: The goal of this study was to determine the transcriptional consequences of norepinephrine transporter (NET) gene deletion in noradrenergic neuron differentiation. The norepinephrine transporter (NET) is the target of powerful mind-altering substances, such as tricyclic antidepressants and the drug of abuse, cocaine. NET function in adult noradrenergic neurons of the peripheral and central nervous systems is that of a scavenger that internalizes norepinephrine from the synaptic cleft. By contrast, norepinephrine (NE) transport has a different role in embryogenesis. It promotes differentiation of neural crest cells and locus ceruleus progenitors into noradrenergic neurons, whereas NET inhibitors, such as the tricyclic antidepressant desipramine and the drug of abuse, cocaine, inhibit noradrenergic differentiation. While NET structure und regulation of NET function is well described, little is known about downstream targets of NE transport. Results: We have determined by long serial analysis of gene expression (LongSAGE) the gene expression profiles of in vitro differentiating wild type and norepinephrine transporter-deficient (NETKO) neural crest derivatives. Comparison analyses with the wild type library (GSM 105765) have identified a number of important differentially expressed genes, including genes relevant to noradrenergic neuron differentiation and to the phenotype of NETKO mice. Furthermore we have identified novel differentially expressed genes. Conclusions: Loss of NET function during embryonic development deregulates signaling pathways that are critically involved in neural crest formation and noradrenergic neuron differentiation. The library was constructed from total RNA of 60 neural crest culture at culture day 7. The neural tubes were dissected from E9.5 embryos that lack the norepinephrine transporter gene.

2008-06-23 | E-GEOD-11788 | biostudies-arrayexpress

High oxygen prevents fetal lethality due to lack of catecholamines

Project description:The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown. When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings. Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses. We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development. Keywords: Comparative with respect to genotype and oxygen conditions

2008-06-03 | GSE10341 | GEO

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