RNA sequencing of norepinephrine- or vehicle-treated mouse colon cancer organoids
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE243326 | GEO | 2024/07/30
REPOSITORIES: GEO
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Project description:RNA sequencing of norepinephrine- or vehicle-treated mouse colon cancer organoids
| PRJNA1017829 | ENA
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.
2011-12-14 | GSE34405 | GEO
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
Project description:Murine small intestinal organoids were stimulated with the general α and β adrenergic receptor agonist norepinephrine and the complete potent and specific α2 adrenergic agonist UK 14,304 (both 1uM) or vehicle controls for 4 days. Afterwards, they were harvested for RNA isolation and proliferation and differentiation gene expression patterns were assessed.
2023-05-09 | GSE230088 | GEO
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
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.
2018-09-05 | GSE106440 | GEO
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
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
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.
2008-06-23 | GSE11788 | GEO
Project description:Chronic stress is associated with hormonal alterations that are known to promote cancer progression. The stress hormone norepinephrine promotes migration and metastasis of prostate cancer cells. Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase which is phosphorylated during chronic stress or norepinephrine treatment. Here, we investigated how norepinephrine modulates the gene expression in Myc-CaP prostate cancer cell line. We also focused on the effect of FAK knockdown in norepinephrine-induced changes of the gene expression profile.
2018-08-29 | GSE119157 | GEO