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Expression data from the human neuroblastoma line SH-SY5Y treated with okadaic acid

ABSTRACT: Okadaic acid (OA) is a widely distributed marine toxin produced by several phytoplank-tonic species and responsible for diarrheic shellﬁsh poisoning in humans. At the molecular level OA is a speciﬁc inhibitor of several types of serine/threonine protein phosphatases.However, the underlying regulatory mechanisms involved in OA-induced cytotoxicity are not well understood. In the present study, we applied a toxicogenomic approach to investigate the effects of OA on gene expression in the human neuroblastoma line SH-SY5Y.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99140 | GEO | 2017/05/23

SECONDARY ACCESSION(S): PRJNA387427

REPOSITORIES: GEO

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A multi-omics approach to elucidate okadaic acid-induced changes in human HepaRG hepatocarcinoma cells

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Time course study of Mediterranean mussel (M. galloprovincialis, Lmk, 1819) digestive gland treated with okadaic acid

Project description:Mytilus galloprovincialis (Lmk, 1819) is economically relevant bivalve specie. In Adriatic Sea, periodical temperatures increases define optimal growth conditions for Dinoflagellate spp which can reach high concentrations also in filter-feeding mussels, thus causing potential human health problems. The most commonly used methods for the detection of Diarrhoeic Shellfish Poisoning biotoxins have either a low sensitivity or are too expensive to be used for routine tests. Genomic tools, such as microarray platforms, provide a reliable and alternative solution to overcome these problems. In this study we used a mussel cDNA microarray for studying gene expression changes in mussels exposed to Okadaic acid. Mussels collected in the Gulf of Trieste, located in Northern Adriatic Sea, were fed with Okadaic acid-spiked invertebrates for five weeks. In a time course experiment we were able to describe an early acute response just from the first 4th day time point. Among the differentially expressed genes we found a general up-regulation of stress proteins and proteins involved in cellular synthesis. Overall, we identified 34 transcripts candidate as useful markers to monitor OA-induced stress in mussels. This study contributes to the characterization of many potential genetic markers that could be used in future environmental monitoring, and could lead to explore new mechanisms of stress tolerance in marine mollusc species. Keywords: Time course, stress response Loop Design experiment including 5 time points (T0 = control samples, T1 = 3 days post treatment, T2 = 1 week post treatment, T4 = 3 weeks post treatment, T6 = 5 weeks post treatment). 3 biological replicates were done for a total number of 15 samples

2010-05-05 | E-GEOD-14885 | biostudies-arrayexpress

Time course study of Mediterranean mussel (M. galloprovincialis, Lmk, 1819) digestive gland treated with okadaic acid

2009-02-19 | GSE14885 | GEO

Argopecten irradians, gills, exposed to okadaic acid

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Analysis of human liver transcriptome after exposure to okadaic acid

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Differences in Toxic Response induced by three Variants of the Diarrheic Shellfish Poisoning Phycotoxins in Human Intestinal Caco-2 Cells

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Project description:Argopecten irradians, gills, exposed to okadaic acid

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Mytilus galloprovincialis, digestive gland and gill, exposed to Prorocentrum lima, producers of okadaic acid.

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2015-11-19 | E-GEOD-72817 | biostudies-arrayexpress

Mytilus galloprovincialis, digestive gland and gill, exposed to Prorocentrum lima, producers of okadaic acid.

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Gene expression during neuronal differentiation in two subtypes of SH-SY5Y

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

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