CDNA microarray data after ATP treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Weihua Li
PROVIDER: E-GEOD-45645 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:A comparative gene expression analysis was performed using cDNA microarray technology in 2B4 and 1E8 cells (subclones derived from PC-3M human prostate carcinoma cell line) to identified the differentially expressed genes between ATP treated and untreated cells
2013-03-30 | GSE45645 | GEO
Project description:Nucleotides triphosphates are extracellular messengers binding to specific plasma membrane receptors (P2Rs) that modulate responses as different as proliferation, differentiation, migration or cell death on several cell types including hematopoietic stem cells. Little and controversial information is available on the role of extracellular nucleotides in human mesenchimal stem cells (hMSCs). In this study, we assessed whether P2Rs are expressed and functional in bone marrow-derived hMSCs. Our results demonstrated, at the mRNA and protein level, the expression of all P2X and P2Y receptor subtypes identified so far. P2R activation by their natural ligands adenosine triphosphate (ATP) and uridine triphosphate (UTP) induced in hMSCs, intracellular Ca2+ concentration changes, plasma membrane depolarization and permeabilization. hMSCs were resistant to the cytotoxic effects of high dose ATP despite the expression of permeabilizing P2Rs as demonstrated by the lack of morphological changes, significant release of intracellular markers of cell death or modification of the mitochondrial network. Gene expression profiling revealed the down-regulation of cell proliferation genes whereas genes involved in cell migration and cytokine production were strongly up-regulated by ATP. Functional studies confirmed the inhibitory activity of ATP on proliferation of hMSCs and clonogenic progenitors. Moreover, ATP exerted a chemotactic effect on hMSCs and increased their migration in response to the chemokine CXCL12. Finally, whereas ATP did not affect T-cell inhibitory activity of hMSCs, the nucleotide increased the production of pro-inflammatory cytokines by hMSCs. Thus, our data show that purinergic signaling modulates hMSC functions and point to a role for extracellular nucleotides on hMSCs biology. hMSCs from 6 healthy donors were seeded at a density of 2.5 x 103 cells/cm2 for 24 hours with or without 1mM ATP. We then assessed the transcriptome profile of ATPM-bM-^@M-^Streated and untreated cells using Affymetrix HG-U133 Plus 2 GeneChip array.
2013-04-11 | E-GEOD-14566 | biostudies-arrayexpress
Project description:Untreated or 20 J/m2 UVC treated RKO cells were collected and RNA from either whole-cell lysates or from polysomal fractions was extracted at 0 (untreated), 3, 6, and 12 h after treatment. RNA from whole-cell lysates or each of 11 polysomal fraction was reverse-transcribed in the presence of [α-33P]dCTP and the radiolabeled product used to hybridize human cDNA arrays. The experiment was repeated using three independent sample sets. The samples were named T-c-A, T-c-B, T-c-C, T-3h-A, T-3h-B, T-3h-C, T-6h-A, T-6h-B, T-6h-C, T-12h-A, T-12h-B, T-12h-C, P-c-1-A, P-c-2-A, P-c-3-A, P-c-4-A, P-c-5-A, P-c-6-A, P-c-7-A, P-c-8-A, P-c-9-A, P-c-10-A, P-c-11-A, P-c-1-B, P-c-2-B, P-c-3-B, P-c-4-B, P-c-5-B, P-c-6-B, P-c-7-B, P-c-8-B, P-c-9-B, P-c-10-B, P-c-11-B, P-c-2-C, P-c-3-C, P-c-4-C, P-c-5-C, P-c-6-C, P-c-7-C, P-c-8-C, P-c-9-C, P-c-10-C, P-c-11-C, P-3h-1-A, P-3h-2-A, P-3h-3-A, P-3h-4-A, P-3h-5-A, P-3h-6-A, P-3h-7-A, P-3h-8-A, P-3h-9-A, P-3h-10-A, P-3h-11-A, P-3h-1-B, P-3h-2-B, P-3h-3-B, P-3h-4-B, P-3h-5-B, P-3h-6-B, P-3h-7-B, P-3h-8-B, P-3h-9-B, P-3h-10-B, P-3h-11-B, P-3h-1-C, P-3h-2-C, P-3h-3-C, P-3h-4-C, P-3h-6-C, P-3h-7-C, P-3h-8-C, P-3h-9-C, P-3h-10-C, P-3h-11-C, P-6h-1-A, P-6h-2-A, P-6h-3-A, P-6h-4-A, P-6h-5-A, P-6h-6-A, P-6h-7-A, P-6h-8-A, P-6h-9-A, P-6h-10-A, P-6h-11-A, P-6h-1-B, P-6h-2-B, P-6h-3-B, P-6h-4-B, P-6h-5-B, P-6h-6-B, P-6h-7-B, P-6h-8-B, P-6h-9-B, P-6h-10-B, P-6h-11-B, P-6h-1-C, P-6h-2-C, P-6h-3-C, P-6h-4-C, P-6h-5-C, P-6h-6-C, P-6h-7-C, P-6h-8-C, P-6h-9-C, P-6h-10-C, P-6h-11-C, P-12h-1-A, P-12h-2-A, P-12h-3-A, P-12h-4-A, P-12h-5-A, P-12h-6-A, P-12h-7-A, P-12h-8-A, P-12h-9-A, P-12h-10-A, P-12h-11-A, P-12h-1-B, P-12h-2-B, P-12h-3-B, P-12h-4-B, P-12h-5-B, P-12h-6-B, P-12h-7-B, P-12h-8-B, P-12h-9-B, P-12h-10-B, P-12h-11-B, P-12h-1-C, P-12h-2-C, P-12h-3-C, P-12h-6-C, P-12h-7-C, P-12h-8-C, P-12h-9-C, P-12h-10-C, P-12h-11-C. ‘T’ represents total RNA, ‘P’ represents RNA from polysomes fractions, ‘c’ represents RNA from untreated cells, ‘3h’ represents RNA from cells collected 3 h after UVC treatment, ‘6h’ represents RNA from cells collected 6 h after UVC treatment, ‘12h’ represents RNA from cells collected 12 h after UVC treatment. The numbers 1-11 correspond to the each polysomal fraction. The letters A, B and C correspond to the three independent experimental datasets. Keywords = post-transcriptional / translation / nascent protein synthesis / stress response / ribonomics Keywords: ordered
2004-06-02 | GSE1440 | GEO
Project description:In the present study, we investigated whether, and to what extent, P2Rs and their ligands are involved in the regulation of AML cells. Our findings show that AML blasts express several receptors belonging to the P2X and P2Y family. Although different samples respond differently to ATP and UTP stimulation (reflecting the variability intrinsic to the group of acute myeloid leukemias), all the tested samples appear to be responsive to purinergic signalling, as demonstrated by intracellular calcium mobilization. GEP analysis demonstrated that ATP induced the expression of cell cycle inhibitors and negative modulators of cell motility, such as inhibitors of GTPase activity. On the contrary, ATP inhibits the expression cell-cycle related genes (cyclins and CDKs), activators of cell motility (Rho GTPases regulators, matrix degradation enzyme and cytoskeleton proteins) and adhesion molecules involved in homing and engraftment. Blast cells obtained from 12 AML patients (3 M0/M1; 3 M2; 3 M4; and 3 M5) were cultured for 24 h with or without 1 mM ATP. Total RNA from 106 ATP-treated and untreated cells was extracted to study variation of gene expression profile induced by ATP treatment in leukemic cells.
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2017-12-20 | E-MTAB-6376 | biostudies-arrayexpress
Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection. Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected. Samples were collected 0, 3, 7, 12, 18 and 24 hpi. There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check). There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi. For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).
2013-05-03 | E-GEOD-45042 | biostudies-arrayexpress
Project description:The experiments were carried out to map the ligand binding landscape of various DNA and RNA duplexed aptamer families. Duplexed Aptamer (DA) constructs were engineered from (i) natural and synthetic DNA and RNA aptamers and (i) synthetic oligonucleotide aptamer-complementary elements synthesized on custom DNA microarrays. The aptamers tested consist of the ATP DNA aptamer, the ATP RNA aptamer, the cocaine DNA aptamer, the human alpha-thrombin DNA aptamer, and the natural add riboswitch aptamer from the pathogenic bacteria Vibrio vulnificus. Each duplexed aptamer family consists of 1000's of synthetic constructs, each formed by hybridizing the aptamer with an aptamer-complementary element (ACE) - here, ACEs consisted of various DNA oligonucleotides synthesized as a custom DNA microarray.
2017-12-20 | E-MTAB-6374 | biostudies-arrayexpress