Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rho kinase paralog regulation of gene transcription

ABSTRACT: The serine/threonine protein kinase paralogs ROCK1 & 2 have been implicated as essential modulators of angiogenesis; however their paralog-specific roles in endothelial function are unknown. Microarray analysis of ROCK knockdown lines revealed overlapping and unique control of global transcription by the paralogs, and a reduction in the transcriptional regulation of just under 50% of VEGF responsive genes. MS1 mouse endothelial cells were stably transfected with non-targeting, ROCK1 specific, or ROCK2 specific shRNA plasmids. Cells were grown to confluence and treated with sham or 2.5 ng/ml human recombinant vascular endothelial growth factor (VEGF) for 12 hours. RNA from six independent biological replicates from each engineered cell line were collected, pooled, and subjected to triplicate technical replicates of microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Brad Bryan

PROVIDER: E-GEOD-34769 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Rho kinase paralog regulation of gene transcription

Project description:The serine/threonine protein kinase paralogs ROCK1 & 2 have been implicated as essential modulators of angiogenesis; however their paralog-specific roles in endothelial function are unknown. Microarray analysis of ROCK knockdown lines revealed overlapping and unique control of global transcription by the paralogs, and a reduction in the transcriptional regulation of just under 50% of VEGF responsive genes.

2012-06-01 | GSE34769 | GEO

Generation of murine stem cells by small molecule

Project description:Transcriptional profiling of stem cells and parental cells Two samples were analyzed: PEG cells and parental cells. Each sample have three replicates.

2015-05-20 | E-GEOD-47102 | biostudies-arrayexpress

Cebpa regulates gene transcription in basophils

Project description:To investigate the mechanisms by which C/EBPa drives basophil differentiation and maintains basophil identity, we examined whether or not C/EBPa promotes basophil molecular programming and simultaneously represses mast cell molecular programming. We performed genome-wide gene expression profiling on basophils and mast cells and found that 6798 genes were shared by mast cells and basophils; 2033 genes were expressed 2-10 (log2 1-3.3)-fold higher in basophils (differentially expressed in basophils); and 413 genes were expressed greater than 10 (log2 3.3)-fold in basophils (highly expressed in basophils). On the other hand, we found 569 genes were expressed 2-10 (log2 -1 to -3.3) fold higher in mast cells and 171 genes were highly expressed in mast cells [greater than 10 fold (log2 -3.3)]. We treated purified basophils prepared from Cebpaf/f RosaYFP/creER mice and Cebpa+/+ RosaYFP/creER control mice with or without 4HT treatment for five days. Gene expression in the treated basophils was analyzed using microarray analysis. Overall, deletion of C/EBPa in basophils resulted in a reduction of mRNA expression for 248 genes and led to an increase in mRNA expression for 255 genes. The majority of the C/EBPa-regulated genes were either differentially or highly expressed in basophils or mast cells. In this study, we compared gene expression in basophils and mast cell and identified genes which specifically expressed in basophils and mast cells. By using Cebpa conditional knock out mice, we identified Cebpa regulated genes in basophils.

2013-04-01 | E-GEOD-41596 | biostudies-arrayexpress

Role of Y1212 VEGFR2 signaling transduction

Project description:The project concerns vascular endothelial growth factor (VEGF) signaling, which is dependent on binding of VEGF to VEGF receptor-2 (VEGFR2) and leads to activation of the receptor kinase and autophosphorylation. Previous mouse studies with the VEGFR-2 phosphorylation site mutation Y1212F showed reduced vascular stability. We here investigate with LC-MS proteomics which signal transduction pathway(s) are lost in the mutant by identifying proteins that bind to the Y1212F site.

2019-08-13 | PXD014517 | Pride

Transcription profiling of human umbilical vein endothelial cells (HUVEC) treated with VEGF-A

Project description:Angiogenesis, the formation of new capillaries by sprouting from preexisting vessels, is mainly induced by VEGF-A. To identify genes which are induced by VEGF-A in endothelial cells, HUVEC were starved and induced by VEGF-A165 for 30, 60 and 150min. RNA of induced and uninduced cells was isolated and subjected to microarray analysis using Affymetrix microarray. Experiment Overall Design: Human umbilical vein endothelial cells were grown in complete EGM-2 medium in dense culture for four days without change of medium and before the stimulation in EGM-2 medium without growth factors over night. The cells were stimulated with 100ng/ml VEGF-A165 for 30, 60 and 150 min. RNA was isolated with Trizol according to the manufacturer's instructions.

2009-10-20 | E-GEOD-15464 | biostudies-arrayexpress

MicroRNA expression in HMVECs: control vs. VEGF-treated vs. PEDF/VEGF-treated

Project description:MicroRNA expression profiling of human microvascular endothelial cells (HMVECs) treated with either vascular endothelial growth factor (VEGF) only or in combination with the natural angiogenesis inhibitor pigment epithelial-derived factor (PEDF). Originally we were interested in the microRNA-mediated regulation of angiogenesis by the endogenous anti-angiogenic PEDF. To identify the microRNAs involved in PEDF signaling in activated endothelial cells, we compared the levels of microRNAs in non-treated microvascular endothelial cells, cells treated with VEGF, and cells treated with a combination of VEGF and PEDF. After treatment, total RNA content was isolated and sent for analysis to LC Sciences, LLC. They performed expression profiling and completed statistical analysis, based on which we confirmed the regulation of one of the microRNAs, mir-27b. In the following experiments, we identified the targets of mir-27b relevant for angiogenesis and confirmed our findings in zebrafish and mouse models. The manuscript describes the key role of mir-27b in determination of the endothelial tip cell fate and venous differentiation by regulating Notch ligand Delta-like ligand 4 (Dll4) and Sprouty homologue 2 (Spry2). Three-condition experiment: untreated (control) HMVECs vs. VEGF-treated HMVECs vs. PEDF/VEGF-treated HMVECs.

2011-12-31 | E-GEOD-34735 | biostudies-arrayexpress

Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

Project description:Transcription profiling of human pulmonary valve endothelial cells treated in culture by VEGF and VEGF+CsA

2010-08-17 | E-TABM-765 | biostudies-arrayexpress

MicroRNAs expression in 20(R)-ginsenoside Rg3-induced anti-angiogenesis

Project description:The angio-suppressive effect of 20(R)-ginsenoside Rg3 (Rg3-R) has been previously demonstrated, and microRNAs (miRNAs) are a vital group of small non-coding RNAs that function as post-transcriptional modulator of gene expression. Thus, using human umbilical vein endothelial cells (HUVEC) as model, we compared the microRNA (miRNA) expression profile of vascular endothelial growth factor (VEGF)-induced cells with the profile of the cell co-treated with VEGF and Rg3-R. Among the screened 553 human miRNAs, 6 up-regulated (miR-520h, miR-487b, miR-197, miR-524*, miR-342 and miR-219) and 3 down-regulated (miR-23a, miR-489 and miR-377) miRNAs were detected in Rg3-R treated vascular endothelial growth factor (VEGF)-induced HUVECs compared to VEGF alone. Real time RT-PCR was subsequently performed to verify the miRNA microarray result. Two condition experiment: VEGF-induced HUVEC and VEGF-induced HUVEC treated with Rg3-R. Three independent microarray experiments, with triplicate per microarray.

2011-09-09 | E-GEOD-31959 | biostudies-arrayexpress

Identification of a biomarker panel for the intake of the common dietary trans fat elaidic acid (trans∆9-C18:1)

Project description:Elaidic acid is an abundant industrial produced trans fatty acid in foodstuffs. Trans fatty acid intake has been correlated to an unfavorable plasma lipoprotein profile and an increased cardiovascular disease risk. The present study aimed to identify a plasma protein biomarker panel related to human intake of elaidic acid. The human liver cell line HepG2-SF was used as a model system, and the cells were maintained for seven days in serum-free medium containing 100 µM elaidic acid (trans∆9-C18:1), oleic acid (cis∆9-C18:1) or stearic acid (C18:0). The secretomes were analyzed by stable isotope labeling of amino acids in cell culture (SILAC), difference in gel electrophoresis (DIGE) and gene expression microarray analysis. Twelve proteins were found to be differentially regulated based on SILAC data (>1.3 fold change, P-value < 0.05), 13 proteins were found to be differentially regulated based on DIGE analysis (>1.3 fold change, P-value < 0.05), and 17 mRNA transcripts encoding extracellular proteins were determined to be affected (>1.3 fold change, P-value < 0.01) following the addition of elaidic acid compared to oleic acid or stearic acid. The results revealed that 37 proteins were regulated specifically in response to elaidic acid exposure, and nine of these proteins were confirmed to be regulated in this manner by using selected reaction monitoring mass spectrometry. HepG2 cells kept used in serum free conditions. The cells were incubated for seven days in either 100 µM oleic, elaidic or stearic acid, before total RNA was extracted. For each group four biological replicates were made and from the each RNA extraction two technical replicates were made. There is a control group without fatty acid incubation.

2011-11-30 | E-GEOD-34045 | biostudies-arrayexpress

Control of VEGF-A trancriptional programs by pausing and genomic compartmentalization

Project description:Vascular endothelial growth factor A (VEGF-A) is a master regulator of vascular development and function. Consequently, VEGF-A regulated gene expression programs have been under heavy research. In this study we study the transcriptional regulation of VEGF-A-responsive genes in primary aortic endothelial cells (HAEC) and vein endothelial cells (HUVEC) using genome wide global run-on sequencing (GRO-Seq). We show that half of VEGF-A induced genes display a paused phenotype under basal conditions and are thus poised for rapid gene activation. Promoters of paused genes are distinguished from those of non-paused by higher basal enrichment for active histone marks H3K4me3, H3K9ac and H3K27ac. We also show that nearly 100% of the VEGF-upregulated genes are induced at the level of elongation, whereas 38-53% are also induced at the level of initiation. We also report a comprehensive chromatin interaction map generated in HUVECs using tethered conformation capture (TCC) and characterize chromatin interactions in relation to transcriptional activity. We demonstrate that sites of active transcription are more likely to engage in chromatin looping and identify chromatin compartments enriched for VEGF-regulated genes. Cell-type specific transcriptional activity was also shown to reflect boundaries of chromatin interactions within the HOXA cluster. Collectively, these findings provide new insight into mechanisms behind VEGF-A-regulated transcriptional programs in endothelial cells. ChIP-Seq (H3K4me2), GRO-Seq and HiC profiling was performed in HUVECs and HAECs.

2014-10-27 | E-GEOD-52642 | 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