Human BE(2)-C neuronal responses to type I IFN stimulation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE16450 | GEO | 2009/07/01
SECONDARY ACCESSION(S): PRJNA122899
REPOSITORIES: GEO
Similar Datasets
Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation. Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks, incubated with universal type I IFN (IFNa-A/D) for 6 or 12 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.
2009-07-12 | E-GEOD-16450 | biostudies-arrayexpress
Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to infection with western equine encephalitis virus (WEEV). Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks and infected with WEEV at an MOI=10 for 6 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.
2009-07-12 | E-GEOD-16451 | biostudies-arrayexpress
Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to infection with western equine encephalitis virus (WEEV).
2009-07-01 | GSE16451 | GEO
Project description:Zika virus (ZIKV) is an emerging, mosquito-borne pathogen associated with a widespread 2015–2016 epidemic in the Western Hemisphere and a proven cause of microcephaly and other fetal brain defects in infants born to infected mothers. ZIKV infections have been also linked to other neurological illnesses in infected adults and children, including Guillain-Barré syndrome (GBS), acute flaccid paralysis (AFP) and meningoencephalitis, but the viral pathophysiology behind those conditions remains poorly understood. Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We perform RNA seq, and global trancriptome analysis to corroborate the effect of retinoic acid in SH-SY5Y cells. Then we analyze the virus infection in differentiated and undifferntiated cells. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation. Enhanced ZIKV infectivity in a neural cell line following differentiation may contribute to viral neuropathogenesis in the developing or mature central nervous system.
2018-10-20 | GSE121534 | GEO
Project description:The human neuroblastoma cell lines SH-SY5Y and IMR-32 can be differentiated into neuron-like phenotypes through treatment with all-trans retinoic acid (ATRA). After differentiation, these cell lines are extensively utilized as in vitro models to study various aspects of neuronal cell biology. However, temporal and quantitative profiling of the proteome and phosphoproteome of SH-SY5Y and IMR-32 cells throughout ATRA-induced differentiation has been limited. Here, we performed relative quantification of the proteomes of SH-SY5Y and IMR-32 cells at multiple time points during ATRA-induced differentiation. The data presented serve as a valuable resource for investigating temporal protein and phosphoprotein abundance changes in SH-SY5Y and IMR-32 cells during ATRA-induced differentiation.
2024-01-24 | PXD046900 | Pride
Project description:The human neuroblastoma cell lines SH-SY5Y and IMR-32 can be differentiated into neuron-like phenotypes through treatment with all-trans retinoic acid (ATRA). After differentiation, these cell lines are extensively utilized as in vitro models to study various aspects of neuronal cell biology. However, temporal and quantitative profiling of the proteome and phosphoproteome of SH-SY5Y and IMR-32 cells throughout ATRA-induced differentiation has been limited. Here, we performed relative quantification of the phosphoproteomes of SH-SY5Y and IMR-32 cells at multiple time points during ATRA-induced differentiation. The data presented serve as a valuable resource for investigating temporal protein and phosphoprotein abundance changes in SH-SY5Y and IMR-32 cells during ATRA-induced differentiation.
2024-01-24 | PXD046871 | Pride
Project description:Neuronal nitric oxide synthase (nNOS/NOS1) is upregulated in the aging brain and contributes to age-and stress-associated neuronal dysfunctions. To mimic this situation for the study of underlying mechanisms we generated a cell model in which human SH-SH5Y neuroblastoma cells constitutively express NOS1 at a level comparable with the rodent brain, whereas the control cells have only low levels. SH-SY5Y cells are the most widely used cell model for neurodegenerative and aging research. They were stably transduced with a lentiviral vector for NOS1 and FACS sorted. Control cells were transduced with the backbone vector, referred to as MOCK or "WT-LV205". Neuronal aging of SH-SY5Y can be imposed with a number of pharmacological, genetic or stress stimuli including retinoic acid and repeated cycles of starvation. Hence, to further challenge the cells we imposed proteostasis stress by treatment with 1 µM rapamycin for 24h or culture in serum-free medium for 24h. Control cells were cultured in full medium, which was RPMI 1640 medium supplemented with heat-inactivated 10% fetal bovine serum, 100 U/ml penicillin/streptomycin, and 2 mM glutamine. All cells were kept at 37°C in 5% CO2 atmosphere in a humidified tissue culture incubator. Rapamycin elicits mTOR dependent autophagy, whereas starvation is a stimulus for chaperone-mediated autophagy, but also affects proteolysis by the proteasome and lysosome and eventually, ER stress. During stimulation, all cells were supplemented with NOS cofactors including 10 µM NAD, 40 µM NADPH, and 100 µM tetrahydrobiopterin. The proteome data set shows nNOS/NOS1-dependent alterations of protein expression in SH-SY5Y neuroblastoma cells in full medium, on stimulation with rapamycin or exposure to serum-free starvation.
2018-10-17 | PXD010538 | Pride
Project description:The main scientific objective of the project was to investigate whether Lamin A/C could be involved in neuroblastoma differentiation. Moreover, taking into account the significance of differentiation stage in the neuroblastoma tumor progression we have also studied a possible role of Lamin A/C in the tumorigenesis of this neuronal cancer. As differentiating stimulus we used the all-trans retinoic acid (RA), the most effective compound which has been shown to induce differentiation in neuroblastoma cells. To get insight into the impairment of cell differentiation produced by the LMNA (Lamin A/C) silencing in SHSY5Y cells, we compared the gene expression profile of control and silenced cells both in Retinoic Acid treated and untreated samples, using the one-color Agilent microarray platform. Four condition experiment: cells infected with a mock vector (Mock cells), treated and untreated with retinoic acid (RA); cells infected with a silencing vector for LMNA (LMNA-KD cells), treated and untreated with retinoic acid.
2013-07-11 | E-GEOD-30677 | biostudies-arrayexpress
Project description:Neuroblastoma is a pediatric tumor that accounts for more than 15% of cancer-related deaths in children. Survival chances for high-risk patients are less than 50%. Retinoic acid treatment is part of the maintenance therapy given to neuroblastoma patients; however, not all tumors respond to retinoic acid-mediated differentiation. Among neuroblastoma tumors, two phenotypically distinct cell types-adrenergic (ADRN) and mesenchymal (MES), have been identified based on their super-enhancer landscape and transcriptional core regulatory circuitries. We hypothesized that distinct super-enhancers in these different tumor cells could mediate differential response to retinoic acid. To this end, we treated four different neuroblastoma cell lines, comprising both ADRN (MYCN amplified and non-amplified) and MES subtypes, with retinoic acid and studied the super-enhancer landscape upon treatment and after removal of retinoic acid. Using H3K27ac ChIP-seq paired with RNA-seq, we compared the super-enhancers in cells that respond to retinoic acid-mediated differentiation versus those that fail to differentiate. We identified unique super-enhancers associated with cells differentiation; however, even among cells that respond to treatment, there was heterogeneity upon removal of retinoic acid, with MYCN amplified cells remaining differentiated whereas MYCN non-amplified cells reverted to a proliferative state. This study identifies regulatory super-enhancers as a plausible mechanism behind the differential response to retinoic acid-mediated differentiation.
2022-07-28 | GSE202239 | GEO
Project description:Neuroblastoma is a pediatric tumor that accounts for more than 15% of cancer-related deaths in children. Survival chances for high-risk patients are less than 50%. Retinoic acid treatment is part of the maintenance therapy given to neuroblastoma patients; however, not all tumors respond to retinoic acid-mediated differentiation. Among neuroblastoma tumors, two phenotypically distinct cell types-adrenergic (ADRN) and mesenchymal (MES), have been identified based on their super-enhancer landscape and transcriptional core regulatory circuitries. We hypothesized that distinct super-enhancers in these different tumor cells could mediate differential response to retinoic acid. To this end, we treated four different neuroblastoma cell lines, comprising both ADRN (MYCN amplified and non-amplified) and MES subtypes, with retinoic acid and studied the super-enhancer landscape upon treatment and after removal of retinoic acid. Using H3K27ac ChIP-seq paired with RNA-seq, we compared the super-enhancers in cells that respond to retinoic acid-mediated differentiation versus those that fail to differentiate. We identified unique super-enhancers associated with cells differentiation; however, even among cells that respond to treatment, there was heterogeneity upon removal of retinoic acid, with MYCN amplified cells remaining differentiated whereas MYCN non-amplified cells reverted to a proliferative state. This study identifies regulatory super-enhancers as a plausible mechanism behind the differential response to retinoic acid-mediated differentiation.
2022-07-28 | GSE201179 | GEO