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
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)
Project description:WGBS 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 followed by 7 days of recovery - day 14)
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®
Project description:Whole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein.
Project description:To investigate whether lncRNAs and mRNAs expression changes in human neuroblastoma cells (SH-SY5Y) following excessive Mn treatment, we have employed whole genome microarray expression profiling.
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.
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.
Project description:Whole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein. Five wt SOD versus five mutant SOD
Project description:This SuperSeries is composed of the following subset Series: GSE21298: Profiling wt SOD versus ALS SOD1(G93A) mutant GSE21305: Profiling neuroblastoma SH-SY5Y with Paraquat treatment Mitochondrial dysfunction has been directly or indirectly implicated in the pathogenesis of a number of neurodegenerative disorders including Parkinson's disease, Alzheimer's disease and Amyotrophic Lateral Sclerosis (ALS). We used exon-sentive microarrays to characterize the responses to different mitochondrial perturbations in cellular models. We examined 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, and SH-SY5Y cells stably expressing the mutant SOD1(G93A) protein, one of the genetic causes of ALS. We identified a common set of genes that have a deregulated transcription and alternative splicing in both models. Noticeably, pathway analysis revealed that the expression of a subset of genes involved in neuritogenesis and axon guidance is perturbed, suggesting that alterations of axonal function may descend directly from mitochondrial damage and be responsible for neurodegenerative conditions. Paraquat treatment on cell lines derived from human neuroblastoma SH-SY5Y and the same cell line stably transfected with cDNAs coding for wild type SOD1 or ALS mutant SOD1 G93A was carried out as described in (Maracchioni et al. J Neurochem 2007, 100, 142-153). Human neuroblastoma SH-SY5Y untransfected or stably transfected with cDNAs coding for wild type SOD1 or the mutant SOD1(G93A) , were cultured in D-MEM/F-12 media with GlutaMAX™ (Gibco, Invitrogen, UK), 10% FBS, 100 Units/ml penicillin G, 100µg/ml streptomycin/ penicillin (Euroclone, Milano, Italy). Stably transfected cells were also maintained in the presence of 400µg/ml Geneticin (G418 sulphate, Euroclone). Cells were fed every 2–3 days and passed once a week. For the microarray experiment, after an initial amplification of each cell type [(SH-SY5Y; SOD1(WT), SOD1(G93A)], cells were aliquoted and cryopreservated in liquid nitrogen. For every experiment an aliquot of each cell line was thawed and seeded. After having reached confluence, cells were reseeded at 3x106cells in 100mm dish. Paraquat (N,N’-dimethyl-4,4’-bipyridinium dichloride, Sigma-Aldrich) treatment was carried out as described in (Maracchioni et al. J Neurochem 2007, 100, 142-153). Total RNA was extracted using TRIzol® Reagent (Invitrogen), and subsequently purified using silica membrane spin columns from RNeasy Mini kit (Qiagen). RNA quantity and purity were assessed using a NanoDrop® instrument (Thermo Fisher Scientific Inc.). Total RNA integrity was assessed by using a 2100 Bioanalyzer (Agilent Technologies) and the RNA Integrity Number (RIN) was calculated. Each condition was replicated 5 times. After extraction and quality check 1.5 µg of total RNA was subjected to removal of ribosomal RNA following the procedure suggested by the manufacturer (Affymetrix). The resulting total RNA was then used to created the biotin-labeled library to be hybridized on GeneChip® Exon 1.0 ST human microarrays following the procedure described by the manufacturer (Affymetrix). The CEL files resulting from the hybridization were analyzed using oneChannelGUI 1.6.5 (Sanges et al. Bioinformatics 2007, 23, 3406-3408). Exon and gene-level probeset summarization was done by mean of RMA and sketch quantile normalization. Gene-level differential expression: to assess differential expression at gene-level, we used an empirical Bayes method together with a false discovery rate (FDR) correction of the p-value Thus, the list of differentially expressed genes was generated using an FDR ≤ 0.05 together with an absolute log2(fold-change) threshold of 1. Exon-level analysis: an intensity filter was subsequently applied at gene-level to remove not expressed and low expressed genes, i.e. genes were retained for exon-level analysis if in all biological replication gene-level signal was greater than 5. Subsequently, only genes characterized to have at least two RNA isoforms annotated in Ensembl database were retained for further analysis. The Splicing Index value was calculated by taking the log2 ratio of the normalized exon intensity (NI) in Sample 1 and the NI in Sample 2. The normalized exon intensity (NI) is the ratio of the probe set intensity to the gene intensity. Alternative splicing events (ASEs) were detected as described in (Della Beffa et al. BMC Genomics 2008, 9, 571).