Transcriptomic profile of normal immortalized fallopian tube cells in response to long-term norepinephrine treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE168097 | GEO | 2021/03/08
REPOSITORIES: GEO
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Project description:The purpose of this study is to understand the effects of adrenergic signaling on the transcriptome of cell line models postulated to be the cells of origin of epithelial ovarian cancers using RNA-Seq. Here we explored the effects of the stress-related hormone, norepinephrine, on normal human ovarian and fallopian tube surface epithelial cellss. We investigated the early transcriptional response to norepinephrine in normal immortalized ovarian surface epithelial cells and fallopian tube secretory cells. RNA-Seq data of treated and untreated cells were analyzed to identify genes with differential expression.
2018-05-25 | GSE108084 | GEO
Project description:To investigate the role of norepinephrine on 3D spheroid formation and survival in early high-grade serous ovarian cancer, we cultured immortalized human fallopian tube epithelial cell lines in ultra-low attachment conditions in the presence or absence of norepinephrine and/or propranolol over 2 different timepoints.
2023-03-27 | GSE228234 | 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:Transcriptomic profile of normal immortalized fallopian tube cells in response to long-term norepinephrine treatment
| PRJNA706023 | ENA
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:Interventions: Phenylephrine (PE):When hypotension occurred,Patients received PE infusion at a starting rate of 5 ml/h of 100µg/ml solution (prepared by diluting 10 mg of PE in 100 ml saline);Norepinephrine (NE):When hypotension occurred,Patients received NE infusion at a starting rate of 5 ml/h of 8 ug/ml solution (prepared by diluting 2 mg NE in 250 ml saline)
Primary outcome(s): First flatus time after surgery;All complications, all-cause mortality, and readmission rates within 28 days after surgery
Study Design: Parallel
| 80763 | ecrin-mdr-crc
Project description:Transcriptional profiling of CD8 Tcm cells comparing untreated control cells to 16 hour norepinephrine treated cells. The goal was to examine the impact of norepinephrine treatment on CD8 Tcm cell global gene expression compared to untreated cells, and also to examine changes that occurred in resting cells and activated cells 24 and 72 hours after stimulation with CD3/28 beads. Two-conditional experiment: Control vs. NE treated CD8 Tcm cells. Biological replicates: 3 replicates for 0 hour and 24 hours, and 2 replicates for 72 hours. Each sample consisted of pooled RNA from 3 different donors.
2015-03-01 | E-GEOD-64635 | biostudies-arrayexpress
Project description:<p>Patients with chronic autonomic failure (CAF) often have disabling orthostatic hypotension (OH). OH in CAF patients is often associated with supine hypertension (hypertension while lying down), which can be severe. Drugs to treat OH worsen supine hypertension. Therefore, the combination of OH with supine hypertension poses a difficult therapeutic challenge. This protocol is a first step toward development of a way to maintain blood pressure during standing without worsening hypertension while lying down. The research question is will a drug (norepinephrine) given intravenously (IV) prevent blood pressure from falling in patients with orthostatic hypotension. </p> <p>This is a placebo controlled, blinded study of 15 patients with neurogenic orthostatic hypotension. The study consists of two experimental days per participant. On a day before the day of norepinephrine (NE) infusion, the patient undergoes head-up tilting while blood pressure is monitored. Tilt angles are increased until the patient has orthostatic symptoms, systolic pressure decreases to less than 90 mm Hg, or systolic pressure decreases by more than 80 mm Hg. On the day of NE infusion patients, receive NE and placebo with the sequence of treatments randomized. If the patient has severe supine hypertension (more than 200 mm Hg systolic), then NE is infused beginning with the patient at whatever tilt angle is required for baseline pressure to be less than 200 mm Hg. NE is infused at doses titrated to keep directly recorded systolic blood pressure at or above the baseline value during exposure to higher tilt angles. When placebo is given, angles of tilt are increased until the patient has orthostatic symptoms, systolic pressure decreases to less than 90 mm Hg, or systolic pressure decreases by more than 80 mm Hg. </p>
| phs001769 | dbGaP
Project description:Early response of human ovarian and fallopian tube surface epithelial cells to norepinephrine
| PRJNA422427 | ENA
Project description:Bacteria can use host hormones as environment cue to modulate their pathogenic processes, which was discovered to play essential role in disease development. Actinobacillus pleuropneumoniae is one of the most important porcine respiratory pathogens causing great economic losses in the pig industry worldwide. Stress factors were found to contribute to the outcome of A. pleuropneumoniae infection. To test whether A. pleuropneumoniae could respond to host stress hormone catecholamines, the gene expression profiles after epinephrine (Epi) and norepinephrine (NE) treatment were compared with the untreated bacteria using microarray. Although the bacterial growth was not affected in the conditions tested, 157 and 104 genes associated with various function categories including many virulence factors were differentially expressed by Epi and NE treatment. 18 common genes were regulated by the two hormones, these genes included genes encoding virulence factors and potential responsors of Epi and NE. Further investigations on virulence traits demonstrated that cytotoxic activity was enhanced by Epi but repressed by NE in accordance with the regulations on apxIA. Biofilm formation was not affected by the two hormones despite that the biofilm formation gene pgaB was affected. Adhesion to host cells was induced by NE but not by Epi, possibly involving other putative adhesins affected by the hormones in addition to the autotransporter adhesin (APL_0443). Our study demonstrated that A. pleuropneumoniae could actively respond to catecholamines to control its virulence traits. The different regulated genes and effects caused by Epi and NE suggested A. pleuropneumoniae may have multiple responsive systems to sense different type of catecholamine hormones. Transcriptional profiles were analyzed using microarray to compared the epinephrine (Epi) or norepinephrine(NE) treated and untreated A. pleuropneumoniae. All samples were harvested from middle exponential phase (4 hours after sub-culture) at the OD600=1.435M-BM-10.065 for control, OD600=1.461M-BM-10.019 for Epi treated strain and OD600=1.545M-BM-10.115 for NE treated strain. Three biological replicates were conducted for each treatment. The total RNA were extracted and hybridized with the whole genome microarray of A. pleuropneumoniae. The signal intensities were normalized and transformed into log2 values. The genes with fold change M-bM-^IM-% 1.5 and P < 0.05 were selected as differentially expressed.
2012-03-19 | E-GEOD-25516 | biostudies-arrayexpress