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Ladostigil attenuates the oxidative and ER stress in human neuroblast-like SH-SY5Y cells

ABSTRACT: Ladostigil attenuates the oxidative and ER stress in human neuroblast-like SH-SY5Y cells

PROVIDER: PRJEB46863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6449730.fastq.gz	Fastqsanger.gz
	ERR6449731.fastq.gz	Fastqsanger.gz
	ERR6449732.fastq.gz	Fastqsanger.gz
	ERR6449733.fastq.gz	Fastqsanger.gz
	ERR6449734.fastq.gz	Fastqsanger.gz

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Similar Datasets

Ladostigil attenuates the oxidative and ER stress in human neuroblast-like SH-SY5Y cells

Project description:In this study, we investigate the impact of ladostigil on neuronal-like SH-SY5Y cells. As ladostigil may attenuate neurotoxicity and cell death that signify chronic stress conditions of an aging brain.

2022-07-25 | E-MTAB-10817 | biostudies-arrayexpress

Ladostigil Attenuates Induced Oxidative Stress in Human Neuroblast-like SH-SY5Y Cells.

Project description:A hallmark of the aging brain is the robust inflammation mediated by microglial activation. Pathophysiology of common neurodegenerative diseases involves oxidative stress and neuroinflammation. Chronic treatment of aging rats by ladostigil, a compound with antioxidant and anti-inflammatory function, prevented microglial activation and learning deficits. In this study, we further investigate the effect of ladostigil on undifferentiated SH-SY5Y cells. We show that SH-SY5Y cells exposed to acute (by H2O2) or chronic oxidative stress (by Sin1, 3-morpholinosydnonimine) induced apoptotic cell death. However, in the presence of ladostigil, the decline in cell viability and the increase of oxidative levels were partially reversed. RNA-seq analysis showed that prolonged oxidation by Sin1 resulted in a simultaneous reduction of the expression level of endoplasmic reticulum (ER) genes that participate in proteostasis. By comparing the differential gene expression profile of Sin1 treated cells to cells incubated with ladostigil before being exposed to Sin1, we observed an over-expression of Clk1 (Cdc2-like kinase 1) which was implicated in psychophysiological stress in mice and Alzheimer's disease. Ladostigil also suppressed the expression of Ccpg1 (Cell cycle progression 1) and Synj1 (Synaptojanin 1) that are involved in ER-autophagy and endocytic pathways. We postulate that ladostigil alleviated cell damage induced by oxidation. Therefore, under conditions of chronic stress that are observed in the aging brain, ladostigil may block oxidative stress processes and consequently reduce neurotoxicity.

| S-EPMC8471141 | biostudies-literature

Transcriptomes in Human neuroblastoma cell line SH-SY5Y under oxidative stress conditions

Project description:The SH-SY5Y Human neuroblastoma cell line was subcloned from the SK-N-SH cell line, which has been isolated from a bone marrow biopsy of a 4 year-old female patient. To examine the overall distribution of gene expression under stress condition in human neuronal cells, we investigated changes in the transcriptome profiles in the SH-SY5Y cells exposed with sodium arsenite which causes oxidative stress. We detected changes in the expression levels for several genes including FOS and Jun, which are well-known stress-dependent upregulated genes.

2023-06-20 | GSE188397 | GEO

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2)

Project description:To investigate atrazine induced transcriptomes in SH-SY5Y cells Total RNA obtained from SH-SY5Y cells were treated with control vehicle (DMSO) or atrazine (ATZ).

2010-10-07 | E-GEOD-24499 | biostudies-arrayexpress

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1)

Project description:To investigate thapsigargin or tunicamycin-induced transcriptomes in SH-SY5Y cells Total RNA was isolated from SH-SY5Y cells were treated with control vehicle (DMSO), thapsigargin (thap) or tunicamycin (tuni).

2010-10-07 | E-GEOD-24497 | biostudies-arrayexpress

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE24497: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1) GSE24499: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2) Refer to individual Series

2010-10-07 | E-GEOD-24500 | biostudies-arrayexpress

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

Expression data from BBEE-treated SH-SY5Y cell

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

Profiling neuroblastoma SH-SY5Y with Paraquat treatment

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

H3K27me3 ChIP-seq in SH-SY5Y human neuroblastoma cell line

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

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