MiRNA & mRNA expression data from fractionated SH-SY5Y cells
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PROVIDER: PRJNA369812 | ENA |
REPOSITORIES: ENA
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Project description:miRNA activity is typically associated with the cytoplasm, but a growing body of evidence suggests non-canonical roles for miRNA in the nucleus. We study miRNA dynamics in neurons and wanted to investigate this possibility in a human neuronal model. We used microarrays to investigate the miRNA composition of the nuclear and cytoplasmic compartments of undifferentiated SH-SY5Y cells.
2017-12-01 | GSE94483 | GEO
Project description:miRNA activity is typically associated with the cytoplasm, but a growing body of evidence suggests non-canonical roles for miRNA in the nucleus. We study miRNA dynamics in neurons and wanted to investigate this possibility in a human neuronal model. We used microarrays to investigate the miRNA and mRNA composition of the nuclear and cytoplasmic compartments of undifferentiated SH-SY5Y cells to identify miRNA-target relationships and networks.
2017-12-01 | GSE94484 | GEO
Project description:MicroRNA (miRNA) has been highlighted in pathogen-host interactions, however, little is known about roles of miRNAs in neurological pathogenesis of human enterovirus 71 (HEV71) infections. In this study, the comprehensive miRNA expression profiling in HEV71-infected human neuroblastoma SH-SY5Y cells were performed to identify cellular miRNAs response to HEV71. A total of 69 miRNAs were differentially expressed in HEV71-infected SH-SY5Y cells compared to non-infected cells. These findings provide new information on the miRNA and mRNA profiles in HEV71 infection, which may serve as a basis for further investigation into the biological functions of miRNAs in the neurological pathogenesis of HEV71 infections. Human neuroblastoma SH-SY5Y cells were infected with HEV71. After infection, the cells were harvested and extracted total RNA for miRNA profiling by hybridization on Affymetrix microarrays. A total of 69 miRNAs were differentially expressed inHEV71-infected SH-SY5Y cells compared to non-infected cells.
2014-07-31 | E-GEOD-45816 | biostudies-arrayexpress
Project description:MicroRNA (miRNA) has been highlighted in pathogen-host interactions, however, little is known about roles of miRNAs in neurological pathogenesis of human enterovirus 71 (HEV71) infections. In this study, the comprehensive miRNA expression profiling in HEV71-infected human neuroblastoma SH-SY5Y cells were performed to identify cellular miRNAs response to HEV71. A total of 69 miRNAs were differentially expressed in HEV71-infected SH-SY5Y cells compared to non-infected cells. These findings provide new information on the miRNA and mRNA profiles in HEV71 infection, which may serve as a basis for further investigation into the biological functions of miRNAs in the neurological pathogenesis of HEV71 infections.
2014-07-31 | GSE45816 | GEO
Project description:Genome wide mRNA and miRNA profiling was performed in SH-SY5Y cells stably overexpressing wild type or mutant MIR204 or MIR618. Mutants came from a large scale genetic screening of brain expressed miRNA genes in patients with schizophrenia or idiopathic generalized epilepsy and in control individuals. Based on enrichment of the variants with the schizophrenic or epileptic phenotype and based on impact prediction, two variants, one near MIR204 (rs7861254) and one in MIR618 (rs2682818) were selected for functional validation. Genome wide profiling of mRNA (micro-array) and mature miRNAs (small RNA sequencing, submitted to SRA) was performed in the created stable cells to assess the effect of the variants and to investigate the function of these miRNA genes. Micro-array analysis on HTA2.0 array was performed at AROS Applied Biotechnology, Denmark. SH-SY5Y cells (purchased from Sigma-Aldrich, catalog number: 94030304-1VL) were transduced with MIR204 or MIR618 wild type or mutant constructs. The stable cells were then split to obtain biological replicates and were cultured separately prior to total RNA extraction and micro-array analysis on the HTA2.0 array. For MIR204 analysis: 2 wt cells versus 3 mutant cells; for MIR618 analysis: 3 wt cells versus 3 mutant cells were used.
2015-11-24 | E-GEOD-69675 | biostudies-arrayexpress
Project description:Background: SH-SY5Y cells exhibit a neuronal phenotype when treated with all-trans retinoic acid (RA), but the molecular mechanism of activation in the signaling pathway mediated by phosphatidylinositol 3-kinase (PI3K) is not sufficiently understood. To shed new light on the mechanism, we comprehensively compared the gene expression profiles between SK-N-SH cells and two subtypes of SH-SY5Y cells (SH-SY5Y-A and SH-SY5Y-E), each of which showed a different phenotype during RA-mediated differentiation. Results: SH-SY5Y-A cells differentiated in the presence of RA, whereas RA-treated SH-SY5Y-E cells required additional treatment with brain-derived neurotrophic factor (BDNF) for full differentiation. In combination with perturbation using a PI3K inhibitor, LY294002, we identified 386 genes and categorized them into two clusters dependent on the PI3K signaling pathway during RA-mediated differentiation in SH-SY5Y-A cells. Transcriptional regulation of the gene cluster was greatly reduced in SK-N-SH cells or partially impaired in SH-SY5Y-E cells in coincidence with a defect in the neuronal phenotype of these cell lines. Additional stimulation with BDNF induced a set of neural genes which were down-regulated in RA-treated SH-SY5Y-E cells but were abundant in the differentiated SH-SY5Y-A cells. Conclusions: We identified the gene clusters controlled by PI3K- and TRKB-mediated signaling pathways during differentiation in two subtypes of SH-SY5Y cells. TRKB-mediated bypass pathway compensates for the impaired neural functions generated by defects in several signaling pathways including PI3K in SH-SY5Y-E cells. The expression profiling data are useful for further studies to elucidate the signal transduction-transcriptional network including PI3K and/or TRKB. Keywords: Cell type comparison, time course
2009-09-01 | GSE9169 | GEO
Project description:Nerve growth factor (NGF) is a neurotrophin that plays an important role in regulating the survival, growth, and differentiation of sympathetic neurons. Many in vitro studies indicate that Egr transcription factors are coupled to NGF signaling and are essential signaling mediators of NGF-dependent differentiation of sympathetic neurons, such as neuroblastoma cells and pheochromocytoma cells. Mice that are deficient for both Egr1 and Egr3 have profound sympathetic nerve system defects, including abnormal neuron degeneration and impaired differentiation (unpublished observations). To further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. The results will be helpful in understanding the pathobiology of those diseases related to aberrant sympathetic neuron differentiation, such as neuroblastoma and dysautonomias, and may provide new insights into therapies for these refractory diseases. To identify NGF-mediated Egr-dependent target genes in human SH-SY5Y/TrkA neuroblastoma cells: Many potential Egr target genes have been described over the years. However, very few have been characterized to be involved in NGF-mediated sympathetic neuron differentiation. In order to further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. Egr1 and Egr3 are rapidly induced after NGF treatment and Egr1 is involved in activation of the differentiation marker gene NPY in SH-SY5Y/TrkA cells. Therefore, SH-SY5Y/TtrkA cells appear to be an excellent model system to study the role of Egr transcription factors in sympathetic neuron differentiation in vitro. A dominant negative Egr molecule that specifically blocks transcriptional activity mediated by Egr transcription factors will be used in this study to identify Egr-dependent target genes. Egr1 and Egr3 are rapidly induced after NGF treatment in human SH-SY5Y/TrkA neuroblastoma cells, which in turn differentiate into sympathetic-like neurons. We hypothesize that Egr transcription factors are involved in activating downstream signaling pathways during NGF mediated differentiation of SH-SY5Y/TrkA cells. Moreover, we hypothesize that by using a dominant negative Egr (dnEgr) molecule that blocks all Egr mediated gene transcription and Affymetrix microarray analysis, it will be possible to identify NGF-mediated Egr transcription dependent gene regulatory networks that may be involved in growth and differentiation of neuroblastoma. An unbiased approach to understanding these gene regulatory networks may lead to new insights relating to NGF signaling involved in neuronal growth and differentiation. Human neuroblastoma SH-SY5Y/TrkA cells will be infected with either dnEgr-expressing adenovirus (SH-SY5Y/TrkA-dnEgr) or with EGFP-expressing control adenovirus (SH-SY5Y/TrkA-EGFP). Equivalent infection efficiency and lack of viral toxicity will be verified by EGFP fluorescence microscopy 24 hours after infection and the cells will be treated with NGF (100 ng/ml). Total RNA will be extracted from SH-SY5Y/TrkA (uninfected), SH-SY5Y/TrkA-dnEgr, and SH-SY5Y/TrkA-EGFP cells treated with NGF for 0, 1 hour and 3 hours. Total RNA will be prepared from all of the samples and a portion subjected to real-time PCR analysis to ensure that NGF mediated Egr gene induction was not altered by the context of viral infection. Pilot experiments demonstrate that Egr genes are still induced in the context of viral infection greater than 100-fold. Egr1 mRNA peak expression is known to occur at 1 hour and decrease by 3 hours after NGF treatment in all of the samples. The peak expression of Egr target genes is expected to occur later than Egr1 peak expression since Egr1 proteins need to be expressed first to initiate the transcription of target promoters. Therefore, the RNA samples from SH-SY5Y/TrkA-dnEgr and SH-SY5Y/TrkA-EGFP treated with NGF for 3 hours will be used to probe Affymetrix high-density human genome U133 Plus 2.0 Arrays to identify differentially expressed genes. RNA amplification for probe synthesis should not be necessary since we will provide 10 ug of intact total RNA for each sample. We will provide three sets of samples to perform the comparative microarray analysis twice from different starting materials and a nine-way comparative analysis of the data will be performed. We expect that cells containing high levels of dnEgr will inhibit NGF mediated Egr-dependent target gene expression and that these gene networks should be identifiable when compared to EGFP infected cells that have normal Egr gene transcriptional activity. Experiment Overall Design: as above
2008-06-12 | E-GEOD-2864 | biostudies-arrayexpress
Project description:Human SH-SY5Y neuroblastoma cells treated with paraquat, a neurotoxic herbicide which both catalyzes the formation of reactive oxygen species (ROS) and induces mitochondrial damage in animal models was profiled using Affimetrix Exon 1.0 ST GeneChips® Human SH-SY5Y neuroblastoma cells was compared with respect to Human SH-SY5Y neuroblastoma cells treated with Paraquat. Parqaut treatment was done as described by Maracchioni, A., Totaro, A., Angelini, D.F., Di Penta, A., Bernardi, G., Carri, M.T., and Achsel, T. (2007) J Neurochem 100, 142-153
2010-12-22 | E-GEOD-21305 | biostudies-arrayexpress
Project description:Gene expression profiling reveals anti-inflammatory effects of BBEE on lipopolysaccharide (LPS)-induced Human neuronal SH-SY5Y cells We evaluated the pretreatment effect of BBEE on LPS-induced inflammation in SH-SY5Y cells. Pretreatment with BBEE could significantly attenuate nitric oxide (NO) production and LPS-induced release of inflammatory mediators in SH-SY5Ycells.
2024-08-31 | GSE270419 | GEO
Project description:H3K27me3 ChIP-seq was performed on: 1) untreated SH-SY5Y human neuroblastoma cells (day 0) 2) vincristine-treated SH-SY5Y human neuroblastoma cells (7 days of treatment - day 7) 3) vincristine-treated SH-SY5Y human neuroblastoma cells (7 days of treatment + 7 days of recover - day 14)
2022-10-01 | E-MTAB-11219 | biostudies-arrayexpress