Secretomic effects of amyloid beta peptides on Alzheimer’s disease related proteins in differentiated SH-SY5Y neuroblastoma cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens (human)
SUBMITTER: Teerakul Arpornsuwan
PROVIDER: PXD045244 | JPOST Repository | Wed Jan 03 00:00:00 GMT 2024
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DMEM+RA+BDNF-1.mgf | Mgf | |||
| DMEM+RA+BDNF-1.mzXML | Mzxml | |||
| DMEM+RA+BDNF-2.mgf | Mgf | |||
| DMEM+RA+BDNF-2.mzXML | Mzxml | |||
| DMEM+RA+BDNF-3.mzXML | Mzxml |
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Project description:SH-SY5Y neuroblastoma cells are widely used as in vitro neuronal model. They can be induced to a differentiated phenotype, presenting neurites and synaptical-like structures in response to retinoic (RA) acid and brain-derived neurotrophic factor (BDNF), providing a model to analyze neuronal differentiation. We report a large scale MS quantification of SH-SY5Y cells proteome during its differentiation process after treatment with RA/BDNF. Using isobaric tags for relative and absolute quantification (iTRAQ) approach and phosphopeptide enrichment protocols, we identified a total of 5587 proteins, 366 of them showed differential abundance between both conditions of culture. Differentiated SH-SY5Y cells showed regulation of proteins and phosphosites strongly related to neuronal development, in contrast, undifferentiated cells expressed proteins more related to cell proliferation and control of cell cycle. Interactive network analysis covered processes as focal adhesion, cytoskeleton dynamics and neurodegenerative diseases and pathway analysis displayed regulation of mitogen-activated protein kinase and phosphoinositide 3-kinase/Akt signaling pathways mainly; the proteins involved in those processes might be considered as markers for neuronal differentiation. Overall the data collection presented here can be explored for any studies which intent to use SH-SY5Y as neuronal model.
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Project description:DNA topoisomerase IIB has an important role in ligand mediated transcriptional regulation of gene expression. SH-SY5Y is a neuroblastoma cell line that can be induced to differentiate into neuronal-like cells in response to retinoic acid. In this study TOP2B has been knocked out using crispr-cas9 to determine the role of TOP2B in the transcriptional response to retinoic acid. RNA was prepared from untreated wild type and TOP2B null SH-SY5Y cells and from cells exposed to 10 uM All Trans Retinoic Acid (ATRA) for 24 hours.
2022-06-28 | GSE142383 | GEO
Project description:Multiple genetic and environmental factors play a role in the development and progression of ParkinsonM-bM-^@M-^Ys disease (PD). The main neuropathological hallmark of PD is the degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SN). To study genetic and molecular contributors to the disease process, there is a great need for readily accessible cells with prominent DAergic features that can be used for reproducible in vitro cellular screening. Here, we investigated the molecular phenotype of retinoic acid (RA) differentiated SH-SY5Y cells using genome wide transcriptional profiling combined with gene ontology, transcription factor and molecular pathway analysis. We demonstrated that RA induces a general neuronal differentiation program in SH-SY5Y cells and that these cells develop a predominantly mature DAergic-like neurotransmitter phenotype. This phenotype is characterized by increased dopamine levels together with substantial suppression of other neurotransmitter phenotypes, such as those for noradrenaline, acetylcholine, glutamate, serotonin and histamine. In addition, we show that RA differentiated SH-SY5Y cells express dopamine and noradrenalin neurotransmitter transporters that are responsible for uptake of MPP(+), a well known DAergic cell toxicant, and that MPP(+) treatment alters mitochondrial activity according to its proposed cytotoxic effect in DAergic neurons. Taken together, RA differentiated SH-SY5Y cells have a DAergic-like phenotype, and provide a good cellular screening tool to find novel genes or compounds that affect cytotoxic processes that are associated with PD. SH-SY5Y cell differentiation process was assessed by comparing RA differentiated and noRA differentiated cells in 8 days of culture. Cells were compared at 6 different time points.
2013-06-01 | E-GEOD-43368 | biostudies-arrayexpress
Project description:Multiple genetic and environmental factors play a role in the development and progression of Parkinson’s disease (PD). The main neuropathological hallmark of PD is the degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SN). To study genetic and molecular contributors to the disease process, there is a great need for readily accessible cells with prominent DAergic features that can be used for reproducible in vitro cellular screening. Here, we investigated the molecular phenotype of retinoic acid (RA) differentiated SH-SY5Y cells using genome wide transcriptional profiling combined with gene ontology, transcription factor and molecular pathway analysis. We demonstrated that RA induces a general neuronal differentiation program in SH-SY5Y cells and that these cells develop a predominantly mature DAergic-like neurotransmitter phenotype. This phenotype is characterized by increased dopamine levels together with substantial suppression of other neurotransmitter phenotypes, such as those for noradrenaline, acetylcholine, glutamate, serotonin and histamine. In addition, we show that RA differentiated SH-SY5Y cells express dopamine and noradrenalin neurotransmitter transporters that are responsible for uptake of MPP(+), a well known DAergic cell toxicant, and that MPP(+) treatment alters mitochondrial activity according to its proposed cytotoxic effect in DAergic neurons. Taken together, RA differentiated SH-SY5Y cells have a DAergic-like phenotype, and provide a good cellular screening tool to find novel genes or compounds that affect cytotoxic processes that are associated with PD.
2013-06-01 | GSE43368 | GEO
Project description:Chemical Checker (CC) is a resource that provides processed, harmonized and integrated bioactivity data on 800,000 small molecules. In the CC, bioactivity data are expressed in a vector format, which naturally extends the notion of chemical similarity between compounds to similarities between bioactivity signatures of different kinds. We experimentally validate that CC signatures can be used to reverse and mimic biological signatures of disease models and genetic perturbations. We developed cellular models of Alzheimer’s disease (AD) by introducing familial AD (fAD) mutations into SH-SY5Y cells. Using CRISPR/Cas9-induced homology-directed repair, we obtained clones harboring the fAD PSEN1-M146V or the APP-V717F mutations. Three compounds (noscapine - 10 uM, palbociclib - 0.4 uM and AG-494 - 10uM) reverted fAD signatures. We confirmed that genes up-regulated in SH-SY5Y fAD mutants were indeed downregulated upon treatment with the drugs, and vice versa. Moreover, the three drug treatments significantly reverted a subset of genes strongly linked to AD, including the recovery of the expression levels of GRIN2D, a glutamate receptor involved in synaptic transmission and BIN1, a gene involved in synaptic vesicle endocytosis and strongly associated with AD risk.
2020-03-17 | GSE137202 | GEO
Project description:Retinoic acid stimulated SH-SY5Y cells are a common model system to study the initial phases of neuronal differentiation. Although these processes are associated with redox-sensitive processes, no comprehensive analysis of oxidative modified cysteines, as one of the main targets for reactive oxygen species, was available. Here, we used quantitative and differential proteomics and redox proteomics, to fill this gap. Our results indicate, that alterations in the redox state very early in the differentiation process, affect the expression of marker proteins and the extension of neurites. The spatiotemporal analysis of reactive oxygen species, suggests a NOX-dependent peak in cytoplasmic O2.-/H2O2 level 2h after retinoic acid stimulation. At the same timepoint 241 out of 275 proteins with an altered cysteine redox state appeared to be reversibly oxidised in the retinoic acid treated samples. Our analyses suggest that redox alterations affect proteins involved in the retinoic acid homeostasis and cytoskeletal dynamics.
2020-03-30 | PXD014381 | Pride
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
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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.
2024-01-24 | PXD046900 | Pride
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.
2024-01-24 | PXD046871 | Pride
Project description:Neuronal nitric oxide synthase (nNOS/NOS1) is upregulated in the aging brain and contributes to age-and stress-associated neuronal dysfunctions. To mimic this situation for the study of underlying mechanisms we generated a cell model in which human SH-SH5Y neuroblastoma cells constitutively express NOS1 at a level comparable with the rodent brain, whereas the control cells have only low levels. SH-SY5Y cells are the most widely used cell model for neurodegenerative and aging research. They were stably transduced with a lentiviral vector for NOS1 and FACS sorted. Control cells were transduced with the backbone vector, referred to as MOCK or "WT-LV205". Neuronal aging of SH-SY5Y can be imposed with a number of pharmacological, genetic or stress stimuli including retinoic acid and repeated cycles of starvation. Hence, to further challenge the cells we imposed proteostasis stress by treatment with 1 µM rapamycin for 24h or culture in serum-free medium for 24h. Control cells were cultured in full medium, which was RPMI 1640 medium supplemented with heat-inactivated 10% fetal bovine serum, 100 U/ml penicillin/streptomycin, and 2 mM glutamine. All cells were kept at 37°C in 5% CO2 atmosphere in a humidified tissue culture incubator. Rapamycin elicits mTOR dependent autophagy, whereas starvation is a stimulus for chaperone-mediated autophagy, but also affects proteolysis by the proteasome and lysosome and eventually, ER stress. During stimulation, all cells were supplemented with NOS cofactors including 10 µM NAD, 40 µM NADPH, and 100 µM tetrahydrobiopterin. The proteome data set shows nNOS/NOS1-dependent alterations of protein expression in SH-SY5Y neuroblastoma cells in full medium, on stimulation with rapamycin or exposure to serum-free starvation.
2018-10-17 | PXD010538 | Pride