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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Hyperosmotic-induced changes in lymphoid cell gene expression

ABSTRACT: We have taken S49 Neo cells (an immature murine T-cell line) through repeated exposures of 500 mOsm Mannitol for 4 hours, killing over 90% of the cells, and then allowed them to recover. After 25 rounds of Mannitol exposure, we observed that these cells now have the ability to volume regulate upon an acute exposure to an osmotic stress, an ability not observed in the parental cell line. Interestingly, we found that these repeated Mannitol treated cells to be resistant to glucocorticoid-induced apoptosis, whereas the parental cell line is highly sensitive to glucocorticoid-induced cell death. The RNA was prepared from cultured cells (~1x106 cells/ml) of the parental cell line S49 Neo and the Mannitol Recovered cell line MR 4-25 using the Qiagen RNeasy mini-kit and including DNase treatment. Three replicates were used for each cell line.

ORGANISM(S): Mus musculus

SUBMITTER: NIEHS Microarray Core

PROVIDER: E-GEOD-62531 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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T-cell development of resistance to apoptosis is driven by a metabolic shift in carbon source and altered activation of death pathways.

Bortner C D CD Scoltock A B AB Cain D W DW Cidlowski J A JA

Cell death and differentiation 20151211 5

We developed a model system to investigate apoptotic resistance in T cells using osmotic stress (OS) to drive selection of death-resistant cells. Exposure of S49 (Neo) T cells to multiple rounds of OS followed by recovery of surviving cells resulted in the selection of a population of T cells (S49 (OS 4-25)) that failed to die in response to a variety of intrinsic apoptotic stimuli including acute OS, but remained sensitive to extrinsic apoptotic initiators. Genome-wide microarray analysis compa ...[more]

PMID: 26658018

Similar Datasets

Hyperosmotic-induced changes in lymphoid cell gene expression

Project description:We have taken S49 Neo cells (an immature murine T-cell line) through repeated exposures of 500 mOsm Mannitol for 4 hours, killing over 90% of the cells, and then allowed them to recover. After 25 rounds of Mannitol exposure, we observed that these cells now have the ability to volume regulate upon an acute exposure to an osmotic stress, an ability not observed in the parental cell line. Interestingly, we found that these repeated Mannitol treated cells to be resistant to glucocorticoid-induced apoptosis, whereas the parental cell line is highly sensitive to glucocorticoid-induced cell death.

2015-12-21 | GSE62531 | GEO

Transcriptome analysis of pathways and drug transporters after hyperosmotic stress of renal MDCK I cells

Project description:Purpose: To perform pathway analysis of MDCK I treated with hyperosmolality and to investigate how hyperosmolality affects the expression of membrane transporters. Method: MDCK I cells were treated for 24 h with medium supplemented with 200 mOsm raffinose, NaCl or urea (total of 500 mOsm). The control was regular medium (300 mOsm). RNA was isolated from 12 replicates from each condition and a cDNA library was prepared using TruSeq RNA Library Preparation Kit v2 from Illumina following the manufacturer's protocol. The sequencing was done with a HiSeq with single read and a length of 51. The alignment was done with Hisat 2, the count with FeatureCount and the statistical analysis with DESeq2. Results: The pathways the cell cycle, the cytokine-cytokine receptor interaction pathway, and the chemokine-signaling pathway were significantly activated in MDCK I cells after treatment of 200 mOsm raffinose or NaCl (total: 500 mOsm), and not 200 mOsm urea, for 24 hours. Several membrane transporters were regulated by hyperosmolality. Conclusion: Hyperosmolality has an inflammatory-like response in MDCK I cells and it also affects the expression of several membrane transporters.

2018-10-31 | GSE110301 | GEO

Global Metabonomic and Proteomic Analysis of Human Conjunctival Epithelial Cells (IOBA-NHC) in Response to Hyperosmotic Stress

Project description:“Dry eye” is a multi-factorial inflammatory disease affecting the ocular surface. Tear hyperosmolarity in dry eye contributes to inflammation and cell damage. Recent research efforts on dry eye have been directed towards biomarker discovery for diagnosis, response to treatment and disease mechanisms. This study employed a spontaneously immortalized normal human conjunctival cell line, IOBA-NHC as a model to investigate hyperosmotic stress-induced changes of metabolites and proteins. Global and targeted metabonomic analyses, as well as proteomic analysis were performed on IOBA-NHC cells incubated in serum-free media at 280 mOsm (control), 380 mOsm and 480 mOsm for 24 h. Twenty-one metabolites and seventy-six iTRAQ-identified proteins showed significant changes under at least one hyperosmotic stress treatment as compared to controls. SWATH-based proteomic analysis further confirmed the involvement of inflammatory pathways such as prostaglandin 2 synthesis in IOBA-NHC cells under hyperosmotic stress. This study is the first to identify glycerophosphocholine synthesis and O-linked β-N-acetylglucosamine glycosylation as key activated pathways in ocular surface cells under hyperosmotic stress. These findings extend the current knowledge in metabolite markers of dry eye and provide potential therapeutic targets for its treatment.

2015-08-17 | PXD002661 | Pride

Global Metabonomic and Proteomic Analysis of Human Conjunctival Epithelial Cells (IOBA-NHC) in Response to Hyperosmotic Stress

2015-08-31 | MTBLS214 | MetaboLights

Post-transcriptional gene regulation following exposure of human articular chondrocytes to hyperosmotic conditions

Project description:Exposing freshly isolated human articular chondrocytes to hyperosmotic conditions (550 mOsm vs 380mOsm controls) for 5 hours and then performing transcriptome analysis using Illumina Ref8 arrays.

2011-03-02 | E-MEXP-3129 | biostudies-arrayexpress

Analysis of the enzymes involved in PEN5 carbohydrate metabolism

Project description:Dr. Eric Vivier's lab would like to tackle the enzymes involved in PEN5 carbohydrate metabolism. We have generated these cell lines by repeated cell sorting and cell cloning of the parental HSB-2 T cell line and the parental JY B cell line. H+ are PEN5+ HSB-2 cells, H- are PEN5- HSB-2 cells; JY+ are PEN5+ HSB-2 cells, JY- are PEN5- HSB-2 cells.

2011-06-14 | GSE29931 | GEO

MetaboLights MTBLS214 - GNPS Global Metabonomic and Proteomic Analysis of Human Conjunctival Epithelial Cells (IOBA-NHC) in Response to Hyperosmotic Stress

Project description:This data set was downloaded from MetaboLights (http://www.ebi.ac.uk/metabolights/) accession number MTBLS214 Abstract:“Dry eye” is a multi-factorial inflammatory disease affecting the ocular surface. Tear hyperosmolarity in dry eye contributes to inflammation and cell damage. Recent research efforts on dry eye have been directed towards biomarker discovery for diagnosis, response to treatment and disease mechanisms. This study employed a spontaneously immortalized normal human conjunctival cell line, IOBA-NHC as a model to investigate hyperosmotic stress-induced changes of metabolites and proteins. Global and targeted metabonomic analyses, as well as proteomic analysis were performed on IOBA-NHC cells incubated in serum-free media at 280 mOsm (control), 380 mOsm and 480 mOsm for 24 h. Twenty-one metabolites and seventy-six iTRAQ-identified proteins showed significant changes under at least one hyperosmotic stress treatment as compared to controls. SWATH-based proteomic analysis further confirmed the involvement of inflammatory pathways such as prostaglandin 2 synthesis in IOBA-NHC cells under hyperosmotic stress. This study is the first to identify glycerophosphocholine synthesis and O-linked ?-N-acetylglucosamine glycosylation as key activated pathways in ocular surface cells under hyperosmotic stress. These findings extend the current knowledge in metabolite markers of dry eye and provide potential therapeutic targets for its treatment.

2017-04-28 | MSV000081036 | GNPS

Glucocorticoid transcriptome in S49 lymphoid cells expressing Bcl2

Project description:S49 (Neo) cells die by apoptosis following dexamethasone (dex) treatment whereas S49 cells expressing Bcl2 are resistant to glucocorticoid-induced cell death. Provocatively, mimicking the loss of intracellular potassium using a low dose of a microbial toxin that acts as a potassium ionophore in combination with dex overcame the resistance afforded by Bcl2 and killed the cells. The ability of the microbial toxin to trigger apoptosis of S49 (Bcl2) cells depends critically on the duration of dex treatment, as a 48-hour dex treatment sensitized the cells to die whereas a 24-hour exposure did not. To determine how the glucocorticoid signaling profile differs at these two time points, we performed RNAseq on RNA isolated from S49 (Neo) cells and S49 (Bcl2) cells treated with and without dex for 24 and 48 hours.

2022-12-28 | GSE210375 | GEO

Effects of murine Oncostatin M on OP9 stromal cells and NIH/3T3 fibroblasts

Project description:The IL-6 cytokine Oncostatin M (OSM) is involved in cell development, growth, hematopoiesis, inflammation and cancer. Intriguingly, OSM has proliferative and antiproliferative effects de-pending on the target cell. The molecular mechanisms underlying these opposing effects are not fully understood and its role in tumorigenesis remains controversial. In the present study, we investigated the effect of murine OSM (mOSM) on proliferation in two cell types of distinct origin. We found that mOSM impairs the proliferation of murine bone marrow (BM) stromal cell lines and primary BM stromal cells, whereas murine fibroblasts responded to mOSM with increased proliferation. When we set out to reveal the mechanisms underlying these opposing effects of OSM on proliferation, we detected increased expression of the OSM receptors OSMR and LIFR in stromal cells. Interestingly, Osmr knockdown and Lifr overexpression attenuated the OSM-mediated effect on proliferation in both cell lines indicating that mOSM affected the pro-liferation of both cell lines signaling mainly through the OSMR. Furthermore, mOSM induced activation of the JAK-STAT, PI3K-AKT and MAPK-ERK pathways in OP9 and NIH/3T3 cells with differences in total protein levels between the two cell lines. Our findings offer new insights into the regulation of proliferation by mOSM.

2021-10-13 | GSE185646 | GEO

miRNASeq of z_Q175 knock-in mouse lines with and without neo cassette

Project description:In order to determine the effect of neoR gene in Q175 locus, miRNASeq was performed to compare the transcriptional signatures of zQ175 knock-in neo-in (z_Q175 KI) (CHDI-81003003) and zQ175 KI neo-out (Z_Q175 (neo -) KI) (CHDI-81003019) mouse lines. The z_Q175 KI is a knock-in mouse line with humanized exon 1 (190-200 pure CAG repeats) derived from Q140 KI colony. It contains floxed neo cassette upstream of exon 1. The Z_Q175 KI (neo -) KI was generated by crossing the Z-Q175 KI line with a zp3-cre transgenic line to delete out the neo cassette.

2018-12-19 | GSE123664 | GEO

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