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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

SUBMITTER: HORVAT Branka

PROVIDER: E-GEOD-32902 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Lethal Nipah virus infection induces rapid overexpression of CXCL10.

Mathieu Cyrille C Guillaume Vanessa V Sabine Amélie A Ong Kien Chai KC Wong Kum Thong KT Legras-Lachuer Catherine C Horvat Branka B

PloS one 20120229 2

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 analyzed the transcriptome profile of NiV infection in primary human umbilical vein endothelial cells. We further assessed some of the obtained results by in vitro and in vivo methods in a hamster model and in brain samples from NiV-inf ...[more]

PMID: 22393386

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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

Project description: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).

2012-10-01 | E-GEOD-33133 | biostudies-arrayexpress

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

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

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.

2012-08-24 | GSE32902 | GEO

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

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

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2016-10-24 | E-GEOD-78020 | biostudies-arrayexpress

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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

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