Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of human HUVEC ells ectotopically expressing K13

ABSTRACT: Integrated microarray and multiplex cytokine analyses of Kaposi's Sarcoma Asssociated Herpesvirus viral FLICE Inhibitory Protein K13 affected genes and cytokines in human blood vascular endothelial cells. The KSHV-encoded K13 protein is one of the few proteins to be expressed in latently-infected spindle cells and the ectopic expression of K13 in human vascular endothelial cells is sufficient to transform them into spindle cells. Experiment Overall Design: We have examined the effect of ectopic K13 expression on global gene expression in human umbilical vein endothelial cells (HUVEC).

ORGANISM(S): Homo sapiens

SUBMITTER: Vasu Punj

PROVIDER: E-GEOD-16051 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Effect of ectotopic expression of K13 on global gene expression in HUVEC

Project description:Integrated microarray and multiplex cytokine analyses of Kaposi's Sarcoma Asssociated Herpesvirus viral FLICE Inhibitory Protein K13 affected genes and cytokines in human blood vascular endothelial cells. The KSHV-encoded K13 protein is one of the few proteins to be expressed in latently-infected spindle cells and the ectopic expression of K13 in human vascular endothelial cells is sufficient to transform them into spindle cells.

2009-08-06 | GSE16051 | GEO

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [RNA-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq (PR infected only -PR only and PR infected followed by ligand treatment-PR+P)

2014-01-01 | E-GEOD-43788 | biostudies-arrayexpress

Endothelial cell proteomic response to Rickettsia conorii infection

Project description:Rickettsia conorii is the etiologic agent of Mediterranean spotted fever, a re-emerging disease with significant mortality. This obligate, gram-negative intracellular pathogen is transmitted via tick bites, resulting in disseminated vascular endothelial cell infection with vascular leakage. In the infected human, Rickettsia conorii infects endothelial cells, stimulating expression of cytokines and pro-coagulant factors. However, the integrated proteomic response of human endothelial cells to R. conorii infection is not known. In this study, we performed quantitative proteomic profiling of R conorii –infected primary HUVECs vs those stimulated with LPS alone.

2015-11-17 | PXD002650 | Pride

Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

Project description:BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways. The sample set is comprised of three biological replicate control human dermal microvascular endothelial cells, and three treated (5 ng/ml human recombinant BMP9) biological replicate human dermal microvascular endothelial cells

2012-09-19 | E-GEOD-40960 | biostudies-arrayexpress

Expression profiles of mRNAs and lncRNAs regulated by let-7e in vascular endothelial cells

Project description:Many studies have demonstrated miRNAs as key regulators of inflammatory responses in endothelial cells (Ecs). However, because of the complexity of inflammatory genes and miRNAs, there would be many undiscovered miRNAs involved in inflammatory responses of ECs. Let-7e is an important member of let-7e family and plays key roles in the regulation of inflammation and endothelial cell proliferation. Furthermore, let-7e expression is significantly increased in many cardiovascular diseases including coronary heart disease. Therefore,we speculated that let-7e might play important roles in the regulation of inflammatory responses in endothelial cells by directly or indirectly targeting certain inflammatory genes. In order to reveal the action of let-7e in vascular endothelial cells, the expression profiles of mRNAs and lncRNAs induced by let-7e in human umbilical vein endothelial cells (HUVECs) were investigated using microarray technology.

2018-12-29 | E-MTAB-4971 | biostudies-arrayexpress

Transcriptome sequencing to identify transcription factor regulatory network and alternative splicing in endothelial cells under VEGF stimulation

Project description:Human umbilical vein vascular endothelial cells (HUVECs) are crucial for angiogenesis that benefits functional recovery after cerebral infarction. This study aims to investigate the mechanisms underlying the effects of vascular endothelial growth factor (VEGF) on HUVECs. HUVECs were treated with 16 ng/mL VEGF165 for 4 days

2015-11-02 | E-GEOD-71216 | biostudies-arrayexpress

Transcription profiling of mouse mECK36: a cell and animal model of virally induced Kaposis sarcoma

Project description:Transfection of a Kaposi's sarcoma (KS) herpesvirus (KSHV) Bacterial Artificial Chromosome (KSHVBac36) into mouse bone marrow endothelial lineage cells generated a cell (mECK36) that induced KS-like tumors in mice. mECK36 formed KSHV-harboring vascularized spindle-cell sarcomas that were LANA+ and displayed a KSHV and host transcriptomes reminiscent of KS tumors. Experiment Overall Design: There are three biological replicates per sample. Tumors (mKS) were compared the the human KS signature. mECK36 and mEC-V were compared to putative BM lineage cells.

2008-06-14 | E-GEOD-6482 | biostudies-arrayexpress

CD109 is novel KSHV entry receptor in human endothelial cells and enhances infection during cellular senescence

Project description:The aging process is characterized by cellular functional decline and increased susceptibility to infections. Understanding the association between virus infection and aging is crucial for developing effective strategies against viral infections in older individuals. Kaposi's sarcoma-associated herpesvirus (KSHV) infection increases the risk of Kaposi's sarcoma, a vascular cancer prevalent among the elderly without HIV infection. However, the relationship between KSHV pathogenesis and cellular senescence remains unknown. Here, we demonstrate that KSHV infectivity is significantly increased in senescent human endothelial cells due to enhanced binding of virions to cell surface. Proteomic analysis identified caveolin-1 and CD109 that promote KSHV infection and were significantly upregulated in senescent cells. In particular, CD109 is expressed on cell surface and directly interacts with KSHV virions to enhance KSHV infection. Knockout of CD109 abolished while overexpression of CD109 promote KSHV binding to cell surface, and infectivity. These results identify CD109 as a novel KSHV entry receptor that enhances KSHV infection in senescent cells, which might in part explain the higher sensitivity of elder subjects to KSHV infection and Kaposi's sarcoma.

2024-04-17 | PXD048212 | Pride

mECK36: a cell and animal model of virally induced Kaposi's sarcoma

2007-01-01 | GSE6482 | GEO

Gene expression timecourse from Dengue virus infected human endothelial cells

Project description:Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease. We used microarrays to investigate the effect of dengue virus infection on gene expression within primary human endothelial cells at various times post infection and identified numerous upregulated antiviral and immune response genes. Early passage primary endothelial cells (HUVECs) were mock infected (no virus) or infected with dengue virus and total RNA collected at 3 timepoints: 12, 24, and 48 hours post infection. Multiple timepoints were analyzed to identify changes in gene expression levels over time. Gene expression from both mock infected and dengue virus infected endothelial cells was evaluated to determine fold induction at each timepoint.

2012-04-10 | E-GEOD-34628 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data