Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA100689 | ENA |
REPOSITORIES: ENA
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Project description:SH-SY5Y cells treated with Quercetin-3-glucoside (10 uM) for 6 hr
| PRJNA100687 | ENA
Project description:SH-SY5Y cells were treated with 6-hydroxydopamine (6-OHDA) to obtain an in vitro PD model. Transcriptome data were collected from both treated and untreated cells.We mapped significantly upregulated genes on a protein-protein interaction network to identify potential drug targets. Drugs targeting the selected drug targets were applied to 6-OHDA treated SH-SY5Y cells. Among the candidate drugs, quercetin and rutin were shown to be neuroprotective by effectively decreasing cell death.
2023-01-01 | GSE198009 | 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
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:Flavonoids are polyphenolic compounds with potent anti-oxidant and free radical scavenging activities. Here, we examined the cytoprotective actions of Quercetin-3-glucoside (Q3G) against oxidative stress induced by hydrogen peroxide. Pre-treatment of the neuroblastoma cells, SH-SY5Y with Q3G for 18 h reduced cell death after a brief exposure to hydrogen peroxide. The cytoprotective effects of Q3G were associated with decreased free radical generation suggesting that this mechanism accounts for Q3G-mediated cytoprotection. To address the possibility that Q3G-mediated cytoprotection involved alterations in gene expression, cDNA microarray studies were performed. These studies identified elevated expression of 25 genes and decreased expression of 3 genes only in Q3G pre-treated cells under oxidative stress. The majority of genes up-regulated by Q3G in SH-SY5Y cells under oxidative stress encode enzymes involved in lipid biosynthesis. Quantitative Real time PCR (qRT-PCR) validated changes in gene expression that were identified by cDNA microarray analyses. The induction of multitude of genes involved in cholesterol signaling pathway by Q3G in cells under oxidative stress suggests an important role for elevated cholesterol synthesis in the cytoprotective actions of Q3G. This hypothesis was confirmed by the detection of elevated levels of cholesterol in cells pre-treated with Q3G and subjected to oxidative stress. Moreover, inhibition of cholesterol biosynthesis with mevastatin blocked the cytoprotective effects of Q3G against oxidative stress-induced cell death. Taken together, these studies suggest a novel mechanism for flavonoid-induced cytoprotection involving elevated cholesterol synthesis that may act to reduce lipid peroxidation and promote membrane repair after oxidative injury. Keywords: cytoprotection, oxidative stress
2006-11-01 | GSE6200 | GEO
Project description:Flavonoids are polyphenolic compounds with potent anti-oxidant and free radical scavenging activities. Here, we examined the cytoprotective actions of Quercetin-3-glucoside (Q3G) against oxidative stress induced by hydrogen peroxide. Pre-treatment of the neuroblastoma cells, SH-SY5Y with Q3G for 18 h reduced cell death after a brief exposure to hydrogen peroxide. The cytoprotective effects of Q3G were associated with decreased free radical generation suggesting that this mechanism accounts for Q3G-mediated cytoprotection. To address the possibility that Q3G-mediated cytoprotection involved alterations in gene expression, cDNA microarray studies were performed. These studies identified elevated expression of 25 genes and decreased expression of 3 genes only in Q3G pre-treated cells under oxidative stress. The majority of genes up-regulated by Q3G in SH-SY5Y cells under oxidative stress encode enzymes involved in lipid biosynthesis. Quantitative Real time PCR (qRT-PCR) validated changes in gene expression that were identified by cDNA microarray analyses. The induction of multitude of genes involved in cholesterol signaling pathway by Q3G in cells under oxidative stress suggests an important role for elevated cholesterol synthesis in the cytoprotective actions of Q3G. This hypothesis was confirmed by the detection of elevated levels of cholesterol in cells pre-treated with Q3G and subjected to oxidative stress. Moreover, inhibition of cholesterol biosynthesis with mevastatin blocked the cytoprotective effects of Q3G against oxidative stress-induced cell death. Taken together, these studies suggest a novel mechanism for flavonoid-induced cytoprotection involving elevated cholesterol synthesis that may act to reduce lipid peroxidation and promote membrane repair after oxidative injury. Keywords: cytoprotection
2006-11-01 | GSE6199 | GEO
Project description:Transcriptome sequencing of human cells (SH-SY5Y)
| PRJNA761138 | ENA