Ontology highlight
ABSTRACT:
PROVIDER: PRJNA683081 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13212132.fastq.gz | Fastqsanger.gz | |||
| SRR13212133.fastq.gz | Fastqsanger.gz | |||
| SRR13212134.fastq.gz | Fastqsanger.gz | |||
| SRR13212135.fastq.gz | Fastqsanger.gz | |||
| SRR13212136.fastq.gz | Fastqsanger.gz |
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Project description:<p>In this study, lymphoblastoid cell line cultures (LCLs) from women with premenstrual dysphoric disorder (PMDD) and asymptomatic controls were compared via whole-transcriptome sequencing (RNA-seq) during untreated (ovarian steroid-free) conditions and after estradiol and progesterone treatment. In untreated LCLs, pathway analysis of the LCL transcriptome revealed, among others, over-expression of ESC/E(Z) complex genes (an ovarian steroid-regulated gene silencing complex) with significant overexpression of MTF2, PHF19, and SIRT1 (P<0.05) in cells from women with PMDD compared with controls. Finally, mRNA expression of several ESC/E(Z) complex genes were increased by progesterone in controls only, and decreased by estradiol in PMDD LCLs. </p>
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Project description:Epstein Barr virus (EBV) nuclear antigen 3C (EBNA3C) is an essential transcription factor for initiating and maintaining human B lymphocyte transformation to lymphoblastoid cell lines (LCLs). To comprehensively identify EBNA3C regulated cell genes in LCLs, oligonucleotide arrays were used to compare RNA abundances in 3 different LCLs transformed by an EBV that conditionally expresses EBNA3C. Cell RNA levels were assessed in actively growing LCLs, under non-permissive or permissive conditions or under non-permissive conditions after transcomplementation with wild type EBNA3C. A two-way ANOVA model with covariates including the 3 different clone effects and the 3 EBNA3C expression levels, identified 550 EBNA3C regulated genes, with False Discovery Rate <0.01 and >1.5 fold change. A seeded Bayesian network analysis of the 80 most significantly EBNA3C regulated genes that changed >1.5 fold, positioned RAC1, LYN and TNF upstream of other EBNA3C regulated genes. Further, Gene Set Enrichment Assay (GSEA) identified EBNA3C regulated genes to be enriched for MAP kinase signaling, cytokine-cytokine receptor interactions, JAK-STAT signaling, and cell adhesion molecule effects, implicating these pathways in LCL growth or survival. Moreover, 106 EBNA3C regulated genes could be placed in protein interaction networks. Since CXCL12 and CXCR4 signaling are implicated in LCL growth and were EBNA3C up-regulated, up-regulation of CXCL12 was validated by qRT-PCR and effects on induced LCL migration were confirmed. EBNA3C regulated genes significantly overlapped with EBNA2 and EBNA3A regulated genes, consistent with a central role for RBP/CSL in these effects.
2011-01-06 | GSE24362 | GEO
Project description:Epstein Barr virus (EBV) nuclear antigen 3C (EBNA3C) is an essential transcription factor for initiating and maintaining human B lymphocyte transformation to lymphoblastoid cell lines (LCLs). To comprehensively identify EBNA3C regulated cell genes in LCLs, oligonucleotide arrays were used to compare RNA abundances in 3 different LCLs transformed by an EBV that conditionally expresses EBNA3C. Cell RNA levels were assessed in actively growing LCLs, under non-permissive or permissive conditions or under non-permissive conditions after transcomplementation with wild type EBNA3C. A two-way ANOVA model with covariates including the 3 different clone effects and the 3 EBNA3C expression levels, identified 550 EBNA3C regulated genes, with False Discovery Rate <0.01 and >1.5 fold change. A seeded Bayesian network analysis of the 80 most significantly EBNA3C regulated genes that changed >1.5 fold, positioned RAC1, LYN and TNF upstream of other EBNA3C regulated genes. Further, Gene Set Enrichment Assay (GSEA) identified EBNA3C regulated genes to be enriched for MAP kinase signaling, cytokine-cytokine receptor interactions, JAK-STAT signaling, and cell adhesion molecule effects, implicating these pathways in LCL growth or survival. Moreover, 106 EBNA3C regulated genes could be placed in protein interaction networks. Since CXCL12 and CXCR4 signaling are implicated in LCL growth and were EBNA3C up-regulated, up-regulation of CXCL12 was validated by qRT-PCR and effects on induced LCL migration were confirmed. EBNA3C regulated genes significantly overlapped with EBNA2 and EBNA3A regulated genes, consistent with a central role for RBP/CSL in these effects. RNAs from three different Lymphoblastoid Cell Lines(LCLs) expressing conditional EBNA3C grown under permissive or non-permissive conditions for 7 days; the same LCLs transcompletemented with EBNA3C expressed in trans at full wild-type level were used to identify EBNA3C regualted cellular genes. Total cell RNAs were hybrdized to Affymetrix U-133 Plus 2.0 microarrays. A two way ANOVA model was developed with covariates including the 3 different clone effects and the 3 EBNA3C expression levels and identified 550 EBNA3C regulated genes.
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Project description:To identify gene expression changes and pathways induced by interferon-? (IFN-?) in B cells, we studied the in vitro response of EBV-transformed B cells (lymphoblast cell lines-LCLs). LCLs were derived from an MS patient repository. Whole genome expression analysis identified 115 genes that were more than two-fold differentially up-regulated following IFN-? exposure, with over 50 novel IFN-? response genes. Pathways analysis demonstrated that IFN-? affected LCLs in a similar manner to other cell types by activating known IFN-? canonical pathways. Additionally, IFN-? increased the expression of innate immune response genes, while down-regulating many B cell receptor pathway genes and genes involved in adaptive immune responses. Several of the novel response genes were tested and validated as IFN-? response genes in human primary B cells. Total RNA from LCL samples treated for four hours with interferon beta (100u/ml) was compared to RNA from untreated LCLs (paired analysis). LCL samples were from patients with MS.
2014-07-30 | E-GEOD-58240 | biostudies-arrayexpress
Project description:Statin-induced gene expression differences observed in LCLs may be influenced by their transformation, and thus differ from those observed in native B-cells. To assess this possibility, we prepared LCLs and purified B-cells from the same donors, and compared mRNA profiles after 24hr incubation with simvastatin (2M-BM-5M) or sham buffer. We prepared LCLs and purified B-cells from the same donors, and compared mRNA profiles after 24hr incubation with simvastatin (2M-BM-5M) or sham buffer. Genes involved in cholesterol metabolism were similarly regulated between the two cell types under both the statin and sham treated conditions, and the statin-induced changes were significantly correlated.
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Project description:In this study, we investigated PPA-induced changes in gene expression profiles of lymphoblastoid cell lines (LCLs) from unaffected individuals, compared with gene expression profiles of LCLs from sex-matched siblings with ASD. Global gene expression profiling analysis revealed that 96 genes in LCLs from the unaffected individuals were significantly altered after PPA exposure, exhibiting expression levels similar to those of their respective siblings with autism. Biological pathway analyses of these PPA-responsive genes suggested significant association with many neurological functions associated with autism, including synaptic transmission, neuronal cell differentiation and apoptosis. Moreover, we demonstrated that PPA also deregulated several of the responsive genes, including APOE, LIFR, NR3C1, and PTK2, in the neuroblastoma cell line SH-SY5Y. Functional analyses further showed that PPA exposure negatively impacted neurite outgrowth and promoted neurodegeneration in the human neuronal cell model. This study indicates that PPA exposure induces global changes in gene expression profiles of LCLs from non-autistic individuals that reflect expression patterns of LCLs from affected individuals.
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Project description:Epstein-Barr virus (EBV) is a herpesvirus that establishes lifelong asymptomatic infection in up to 95% of the human population. In vitro EBV infection of resting B lymphocytes drives them to proliferate as lymphoblastoid cell lines (LCLs). EBV expresses limited genes, which include six nuclear proteins (EBNAs), three integral membrane proteins (LMPs), and more than 30 micro RNAs in LCLs. EBNA3C, one of the six nuclear proteins, is transcription factor and regulates host cell genes. The growth effects of EBNA3C appear to be primarily due to suppression of the CDKN2A gene products, p16INK4A and p14ARF. Conditional inactivation of EBNA3C results in increasing p16 expression and this is accompanied by the substantial reduction of the repressive H3K27me3 modification at the CDKN2A promoter and cell cycle arrest. To further elucidate the relationship between EBNA3C and H3K27me3 modification, we profiled H3K27me3 by ChIP-seq in CDKN2A knockout EBNA3CHT LCLs in the presence (4HT+) or absence (4HT-) of 4-hydroxytamoxifen, with a total of 4 biological replicates per condition.
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