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Gene expression profiling of Human Umbilical Vein Endothelial Cells (HUVEC) after treatment with Erg or control antisense (GeneBloc)

ABSTRACT: The endothelial transcription factor Erg (Ets Related Gene) plays an important role in homeostasis and angiogenesis by regulating many endothelial functions including survival and junction stability. Here we show that Erg regulates endothelial cell migration. Transcriptome profiling of Erg-deficient endothelial cells (EC) identified 80 genes involved in cell migration as candidate Erg targets, including regulators of the Rho GTPases. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVEC) resulted in decreased migration in vitro, whilst Erg over-expression using adenovirus caused increased migration. Live-cell imaging of Erg-deficient HUVEC showed a reduction in lamellipodia, in line with decreased motility. Both actin and tubulin cytoskeletons were disrupted in Erg-deficient EC, with a dramatic increase in tubulin acetylation. Amongst the most significant microarray hit was the cytosolic histone deacetylase (HDAC)-6, a regulator of cell migration. Rescue experiments confirmed that HDAC6 mediates the Erg-dependent regulation of tubulin acetylation and actin localization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32984 | GEO | 2012/02/27

SECONDARY ACCESSION(S): PRJNA146439

REPOSITORIES: GEO

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Gene expression profiling of Human Umbilical Vein Endothelial Cells (HUVEC) after treatment with Erg or control antisense (GeneBloc)

Project description:The endothelial transcription factor Erg (Ets Related Gene) plays an important role in homeostasis and angiogenesis by regulating many endothelial functions including survival and junction stability. Here we show that Erg regulates endothelial cell migration. Transcriptome profiling of Erg-deficient endothelial cells (EC) identified 80 genes involved in cell migration as candidate Erg targets, including regulators of the Rho GTPases. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVEC) resulted in decreased migration in vitro, whilst Erg over-expression using adenovirus caused increased migration. Live-cell imaging of Erg-deficient HUVEC showed a reduction in lamellipodia, in line with decreased motility. Both actin and tubulin cytoskeletons were disrupted in Erg-deficient EC, with a dramatic increase in tubulin acetylation. Amongst the most significant microarray hit was the cytosolic histone deacetylase (HDAC)-6, a regulator of cell migration. Rescue experiments confirmed that HDAC6 mediates the Erg-dependent regulation of tubulin acetylation and actin localization. The functional role of Erg in EC was studied by gene expressing profiling using three separate HUVEC isolates treated with either control antisense or Erg-specific antisense for 24 or 48 hours.

2012-02-27 | E-GEOD-32984 | biostudies-arrayexpress

Expression data from ERG Si treated and Control HUVEC cells

Project description:ERG (Ets Related Gene) is an ETS transcription factor that was originally described for its role in a number of human cancers. Our preliminary data demonstrate that ERG exhibits a highly EC restricted pattern of expression in cultured primary cells and several adult tissues including the heart, lung, and brain. In response to inflammatory stimuli, such as TNF-alpha, we observed a marked reduction of ERG expression in EC. To further define the role of ERG in the regulation of normal EC function we used RNA interference to knockdown ERG. Knockdown of ERG in human umbilical vein EC (HUVEC) using siRNA was associated with the reduction of a number known ERG targets. Keywords: SIRNA Functional Role

2009-04-17 | GSE14801 | GEO

ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.

2022-07-05 | PXD033447 | Pride

Long non-coding RNA profiling in 6 cell types

Project description:To identify endothelial cell (EC)-enriched long noncoding RNAs (lncRNAs), gene expression analysis was conducted on two EC cell types and 4 non-EC cell types. Specifically, the EC cell types were human umbilical vein endothelial cells (HUVEC) and human dermal microvascular endothelial cells (HMVEC). The 4 non-EC cell types were human aortic smooth muscle cells (HASMC), Fibroblasts, Hepatocytes, and keratinocytes. Of the 23 155 putative lncRNAs represented in the custom lncRNA microarrays, 18 524 lncRNAs were found to be expressed above the 20% percentile in at least one cell type. Importantly, 28 EC-enriched lncRNAs were identified in common between HUVEC and HMVEC with 28 and 59 enriched uniquely in either HUVEC or HMVEC, respectively. Of interest, STEEL, an EC-enriched lncRNA was identified and its role in EC biology was further characterized.

2018-03-30 | GSE108318 | GEO

The transcription factor ERG regulates super-enhancers in endothelial cells [ERG siRNA]

Project description:We provide the functional and epigenomic evidence for ERG binding to super-enhancers in HUVEC and further show that loss of ERG results in inhibition of specific endothelial super-enhancers and associated target genes.

2019-03-22 | GSE124892 | GEO

The transcription factor ERG regulates super-enhancers in endothelial cells [ERG ChIP-seq]

2019-03-22 | GSE124891 | GEO

Single cell RNA-Seq analysis provide deeper molecular insights into abnormal maturation of tubastatin A-treated mouse oocytes

Project description:In our previous study, we observed that Tub-A treatment induced an increased level of the acetylation of alpha-tubulin, and a failure of spindle migration and actin cap formation. Most Tub-A treated oocytes were arrested in an MI-like or a GVBD-like stage and decreased mTOR (spindle formation factor) and mDia1 (inhibitor of actin assembly) in an HDAC6 expression-dependent manner. We wonder if TubA only affects HDAC6 expression. Therefore the purpose of this study is to clarify the cause of the phenomenon through RNA-seq analysis.

2018-11-30 | GSE115008 | GEO

Dynamic regulation of VEGF-inducible genes by an ERK-ERG-p300 transcriptional network

Project description:Effect of ERG knockdown, with and without VEGF stimulation, on vascular endothelial cell (HUVEC) gene expression

2017-06-15 | E-MTAB-5207 | biostudies-arrayexpress

Expression profiling of Endothelial (EC) and Non-endothelial Cells

Project description:Gene expression profiling of HUVEC (human umbilical vein EC cell; Lonza), HAEC (human aortic EC cells), HCAEC (human coronary artery EC cells), HPAEC (human pulmonary artery EC cells), HMVEC (human microvascular (dermal) , HASMC ( Human Aortic Smooth Muscle Cells), T cells and Bcells. Gene expression profiling of Endothelial cells and Non-endothelial cells in order to identify the genes with preferntial expression to endothelial cells. The experiments are performed in duplicate on both the HT Human Genome U133A and U133B arrays.

2011-04-04 | E-GEOD-21212 | biostudies-arrayexpress

KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [RNA-seq]

Project description:Transcription factors (TFs) engage in various cellular essential processes including differentiation, growth and migration. However, the master TF involved in distant metastasis of nasopharyngeal carcinoma (NPC) remains largely unclear. Here we show that KLF5 regulates actin remodeling to enhance NPC metastasis. We analyzed the msVIPER algorithm-generated transcriptional regulatory networks and identified KLF5 as a master TF of metastatic NPC linked to poor clinical outcomes. KLF5 regulates actin remodeling and lamellipodia formation to promote the metastasis of NPC cells in vitro and in vivo. Mechanistically, KLF5 preferentially occupies distal enhancer regions of ACTN4 to activate its transcription, whereby decoding the informative DNA sequences. ACTN4, extensively localized within actin cytoskeleton, facilitates dense and branched actin networks and lamellipodia formation at the cell leading edge, empowering cells to migrate faster. Collectively, our findings reveal that KLF5 controls robust transcription program of ACTN4 to modulate actin remodeling and augment cell motility which enhances NPC metastasis, and provide new potential biomarkers and therapeutic interventions for NPC.

2024-04-18 | GSE243952 | GEO

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