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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Analysis of the early transcriptome signature of infection of primary endothelial cells by Nipah virus vs. Nipah virus deleted for the expression of non-structural C protein

ABSTRACT: Nipah virus (NiV) is a highly pathogenic, negative strand RNA paramyxovirus that has recently emerged from flying foxes to cause serious human disease. To study the poorly-understood role of nonstructural NiV proteins in NiV pathogenesis, we generated recombinant viruse lacking the expression of accesory NiV C protein (NiVM-bM-^HM-^FC). To analyse the molecular basis of NiVM-bM-^HM-^FC attenuation we have used the gene microarray approach to study early changes of gene expression in infected primary human endothelial cells, which is a major cellular target of human NiV infection. We performed microarray gene expression profiling of NiV infected HUVEC cell (2 replicates), of uninfected HUVEC cell (2 replicates) and of NiVM-bM-^HM-^FC infected HUVEC cell (2 replicates).

ORGANISM(S): Homo sapiens

SUBMITTER: HORVAT Branka

PROVIDER: E-GEOD-33133 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Analysis of the early transcriptome signature of Nipah virus infection in primary endothelial cells

Project description:Nipah virus (NiV) is a recently emerged zoonotic Paramyxovirus that causes regular outbreaks in East Asia with mortality rate exceeding 75%. Major cellular targets of NiV infection are endothelial cells and neurons. To better understand virus-host interaction, we analysed the transcriptome profile of NiV infection in primary human umbilical vein endothelial cells. We found that NiV infection strongly induces genes involved in interferon response in endothelial cells. Among the top ten upregulated genes, we identified the chemokine CXCL10 (interferon-induced protein 10, IP-10), an important chemoattractant involved in the generation of inflammatory immune response and neurotoxicity. We performed microarray gene expression profiling of NiV infected HUVEC cell (2 replicates) and of uninfected HUVEC cell (2 replicates).

2012-08-24 | E-GEOD-32902 | biostudies-arrayexpress

Microarray gene expression profiling in central neurocytomas

Project description:Microarray gene expression profiling of central neurocytomas (CNs). Comparison between neurocytoma, pineocytoma (PC) and pineoblastoma (PB) relative to normal brain. Gene expression analysis was performed on tumor samples. Tumor tissues of 5 CNs, 2 PCs (low-grade pineal parenchymal tumors (PPTs)) and 2 PBs (high-grade PPTs) were obtained from the NeurobiotecBank (Groupement Hospitalier Est, Bron, France) or from the AP-HM Tissue Bank (Assistance Publique-HM-CM-4pitaux de Marseille, France). At surgery, the tumor tissue was divided into 2 fragments, one of which was frozen and stored in liquid nitrogen for RNA extraction, whereas the other was fixed for histopathologic analysis.

2013-02-19 | E-GEOD-35499 | biostudies-arrayexpress

The Refilin/Filamin complex regulates filipodia dynamics in oligodendrocyte progenitor cells.

Project description:Actin assembly and dynamics control the shape, motility and functions of diverse cell types. Programme for controlling theses dynamics is hard-coded into actin binding proteins and regulatory proteins. Refilins (RefilinA and RefilinB) are short lived regulatory proteins that interact with the actin-binding protein Filamin to convert it from an actin branching protein into one that bundles. We here show that different mechanisms converge to increase Refilin level in brain NG2+ precursor cells (polydendrocytes) committed to differentiate into the oligodendrocyte lineage. RefilinA is up-regulated through transcriptional activation during commitment into oligodendrocyte progenitor cells (OPC). RefilinB expression relies on PDGF signalling and is further stabilized by a unique auto-inhibitory domain masking the adjacent conserved PEST degradation signal. In NG2+ precursor cells and OPC, the RefilinB/Filamin complex localizes on filipodia protrusions and filipodial processes. Stable ectopic expression of Refilins in cells stimulates membrane remodelling dynamics linked with filipodia growth. These studies extend the function of the Refilin/FLNA complex to cell membrane remodelling linked with reorganization of underlying actin cytoskeleton. We performed whole transcriptomic analysis on the three cell population derived from OPC cells. Three different cultures were done and for each experiment we compared each cell population (NG2+, NG2+/A2B5 and O4) to the other 2 cell populations.

2013-05-01 | E-GEOD-37600 | biostudies-arrayexpress

Transcriptomic dysregulation in aggressive and malignant prolactin tumours

Project description:Pituitary tumours are generally benign. However, many are invasive and some of these are aggressive with high proliferation and recurrence rates. Only metastatic tumours are considered malignant and are rare (0.2%). To identify molecular events associated with the aggressive and malignant phenotypes, we combined a comparative genomic hybridization and transcriptomic analysis of 13 prolactin (PRL) tumours classified as non-invasive (NI; n=5), invasive (I; n=2) or aggressive-invasive (AI; n=6). Each tumour showed copy number alterations which appeared to be varied and discrete in the NI and I tumour groups, and more numerous and extensive in the AI tumour group. Allelic loss within the p arm region of chromosome 11 was detected in five of the AI tumours. This region contains the cytobands 11p15.2, 11p15.1, 11p14.3, 11p14.2, 11p14.1, 11p13, 11p12 and 11p11.2. Furthermore, an allelic loss in the 11q arm was also observed in three of these five tumours, which were considered malignant based on the presence of metastases. The comparison of genomic and transcriptomic data showed that allelic loss impacted upon the expression of genes located in the imbalanced region. An original data filtering strategy allowed us to highlight five genes (DGKZ, CD44, TSG101, GTF2H1 and HTATIP2), within the missing 11p region, potentially responsible for triggering the aggressive and malignant phenotypes of PRL tumours. Our novel combined genomic and transcriptomic analysis underlines the importance of chromosome 11 allelic loss in aggressive and malignant PRL tumours and led us to propose a new strategy to find markers of progression in rare tumours. Transcriptomic analysis of Codelink Human Whole Genome Bioarray was performed for 13 prolactin tumors: 6 aggressive-invasive, 2 invasive, and 5 non-invasive.

2011-03-16 | E-GEOD-22812 | biostudies-arrayexpress

gene expression profiling in CD69 positive blood cells selected from Healthy blood Donors and HTLV-1-infected patients

Project description:The goal of the study was to identify difference in gene expression between activated /CD69+ blood cells selected from HTLV-1-infected patient displaying HAM-TSP disease (HTLV-1-associated myelopathy/tropical spastic paraparesis), compared to healthy blood donor /HD (biological sample providers: Dr. Antoine Gessain, Pasteur Institute Paris and Etablissement FranM-CM-'ais du Sang) We performed microarray gene expression profiling of Immune cells selected on the marker of early activation, CD69, by the use of MACS beads (Miltenyi Biotec), from 10.106 blood cells of two healthy blood donors and two HAM/TSP patients

2012-03-14 | E-GEOD-33859 | biostudies-arrayexpress

CCN5, a novel transcriptional repressor

Project description:CCN5 is a member of the CCN (Connective Tissue Growth Factor/Cysteine-rich 61/Nephroblastoma overexpressed) family and was identified as an estrogen-inducible gene in estrogen receptor-positive cell lines. However, the role of CCN5 in breast carcinogenesis remains unclear. We report here that CCN5 protein is localized mostly in the cytoplasm, and in part in the nucleus, of human tumor breast tissue. Using a heterologous transcription assay, we demonstrate that CCN5 can act as a transcriptional repressor, presumably through association with histone deacetylase HDAC1. Microarray gene expression analysis showed that CCN5 represses expression of genes associated with epithelial-mesenchymal transition (EMT) as well as expression of key components of the TGF-beta signaling pathway, prominent among them TGF-betaRII receptor. We show that CCN5 is recruited to the TGF-betaRII promoter, thereby providing a mechanism by which CCN5 restricts transcription of the TGF-betaRII gene. Consistent with this finding, we found that CCN5 functions to suppress TGF-beta-induced transcriptional responses and invasion that is concomitant with EMT. Thus, our data uncovered CCN5 as a novel transcriptional repressor that plays an important role in regulating tumor progression functioning, at least in part, by inhibiting the expression of genes involved in the TGF-beta signaling cascade that is known to promote EMT. We performed microarray gene expression profiling of one MCF-7-sh-CCN5 sample and one MCF-7-sh-scrambled sample (control sample).

2011-11-30 | E-GEOD-25431 | biostudies-arrayexpress

Genomic alterations of chromosome 11 induce transcriptome dysregulation in aggressive and malignant prolactin tumours

Project description:This SuperSeries is composed of the following subset Series: GSE22615: Genomic alterations of chromosome 11 induce transcriptomic dysregulation in aggressive and malignant prolactin tumours GSE22812: Transcriptomic dysregulation in aggressive and malignant prolactin tumours Refer to individual Series

2011-09-15 | E-GEOD-32191 | biostudies-arrayexpress

Aspergillus nidulans strains TNO2a3, M-bM-^HM-^FsnfA and M-bM-^HM-^FschA grown on avicel as sole carbon source

Project description:Transcriptome of A. nidulans TNO2a3, M-bM-^HM-^FsnfA and M-bM-^HM-^FschA strains when grown on complete media (CM) and transferred to minimal media plus avicel as a sole carbon source for 8 and 24 hours. Three conditions: complete media (reference) for 24h, and minimal media plus avicel for 8 and 24 hours. Three strains: TNO2a3, M-bM-^HM-^FsnfA and M-bM-^HM-^FschA. Three biological repetitions of each timepoint of TNO2a3 and M-bM-^HM-^FschA, and two for each timepoint of M-bM-^HM-^FsnfA.

2013-07-16 | E-GEOD-47810 | biostudies-arrayexpress

Aspergillus nidulans strains TNO2A3, M-bM-^HM-^FmsbA and M-bM-^HM-^FMHD grown in complete media (YUU) and on avicel as sole carbon source

Project description:Transcriptome of A. nidulans TNO2A3, M-bM-^HM-^FmsbA and M-bM-^HM-^FMHD strains when grown on complete media (YUU) and transferred to minimal media plus avicel as a sole carbon source for 24 hours Two conditions: complete media (reference) for 24h and minimal media plus avicel for 24 hours. Three strains TNO2A3, M-bM-^HM-^FmsbA and M-bM-^HM-^FMHD. Three biological repetitions of each point.

2015-01-01 | E-GEOD-60594 | biostudies-arrayexpress

Statistical analysis of differential gene expression relative to a fold change threshold on NanoString data of mouse odorant receptor genes

Project description:We developed a systematic statistical method, tTREAT, to identify differentially expressed genes with respect to a predefined FC threshold. The tTREAT approach aims to reduce false discoveries. We applied statistical tests relative to a Fold Change threshold to a dataset about mouse odorant receptor gene expression generated by the NanoString technology. We used mouse strains M-bM-^HM-^FP and M-bM-^HM-^FH that lack the P element and the H element respectively. We also used a mouse strain generated by chromosome engineering (M-bM-^HM-^FOlfr7M-bM-^HM-^F) whereby a 2.4 Mb region is deleted, thus lacking 99 odorant receptor genes. We sought to understand the regulation of the expression of odorant receptor genes by comparing mutant mice to wildtype mice.

2014-01-08 | E-GEOD-53876 | biostudies-arrayexpress

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