GEO DataSets

Analysis of HUVECs stimulated with two important angiogenic stimuli: peroxisome proliferator-activated receptor (PPAR) β/δ agonist and hypoxia. Results provide insight into possible synergistic molecular interactions between the PPAR β/δ and hypoxia-inducible factor (HIF) 1 signaling pathways.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 agent, 2 stress sets

Platform:

GPL570

Series:

GSE50378

4 Samples

Download data: CEL

(Submitter supplied) Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS5633

Platform:

GPL570

4 Samples

Download data: CEL

(Submitter supplied) H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL10999

22 Samples

Download data: WIG

(Submitter supplied) H3K27Ac is one of the expressed enhancer markers in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for H3K27ac, and performed ChIP-seq to identify H3K27ac binding site in whole genome manner under hypoxia.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

2 Samples

Download data: BED, WIG

(Submitter supplied) Differential gene expression profiles were observed in response to Hras in either wild-type or Ppar-beta null primary keratinocytes and differentail gene edxpression profiles by GW0742 were only found in wild-type keratinocytes.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

24 Samples

Download data: CEL

(Submitter supplied) Alcoholic liver disease is a pathological condition caused by over-consumption of alcohol. Due to the high prevalence of morbidity and mortality associated with this disease, there remains a need to elucidate the molecular mechanisms underlying the etiology to develop new treatments. Since peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) modulates ethanol-induced hepatic effects, the present study examined alterations in gene expression that may contribute to this disease.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

12 Samples

Download data: CEL

(Submitter supplied) We report the high-throughput profilings of HIF1 and histone modifications in human umbilical vein endothelial cells (HUVEC). By obtaining over two billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of HUVEC under normoxia and hypoxia. We find that HIF1binds to not only to transcriptional starting sites but also enhancer regions and that HIF1 binding sites were overlapped with lysine 4 trimethylatio, monomethylation and lysine 27 acetylation . more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

8 Samples

Download data: BED, WIG

(Submitter supplied) Total 23 samples were derived from [1] HUVEC treated in the absence (0h) or presence of hypoxia (1, 2, 4, 8, 12, and 24 hrs) to determine hypoxia-regulated gene in endothelial cells, [2] control siRNA or HIF1α siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [3] control siRNA or KDM3A siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [4] ChIP-seq data for HIF1 binding sites and histone modifications under normoxia and hypoxia in endothelial cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

15 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platforms:

GPL6246 GPL7440

34 Samples

Download data: CEL

(Submitter supplied) Little is known about the role of the transcription factor PPARß/d in liver. Here we set out to better elucidate the function of PPARß/d in liver by comparing the effect of PPARa and PPARß/d deletion using whole genome transcriptional profiling and analysis of plasma and liver metabolites. In fed state, the number of genes altered by PPARa and PPARß/d deletion was similar, whereas in fasted state the effect of PPARa deletion was much more pronounced, consistent with the pattern of gene expression of PPARa and PPARß/d. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

16 Samples

Download data: CEL

(Submitter supplied) Reduced or absent cytotrophoblast invasion of the maternal uterine spiral arteries is a common clinical finding in studies of pregnancies complicated by preeclampsia, suggesting that the mechanisms behind invasion of these cells is perturbed. The placenta initially develops in a low oxygen environment of 1-2% oxygen until after the 10th week of pregnancy. During this time oxygen concentration exerts a major influence over trophoblast activity and, in vitro, hypoxia inducible factors are proposed to be one of many key regulators of first trimester trophoblast behaviour. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

18 Samples

Download data: IDAT

(Submitter supplied) HUVECs were stimulated and samples were prepared after 0 and 30 min. Chromatin interaction mediated by active RNA polymerase II was detected by ChIA-PET.

Organism:

Homo sapiens

Type:

Other

Platform:

GPL10999

4 Samples

Download data: TSV

(Submitter supplied) KLF2 and KLF4 are important transcriptional factors in endothelial cells, however their roles in statin treatment has not been elucidated. Here we report the comprehensive change of transcripts of statin treated HUVECs transfected with siRNA KLF2 or KLF4. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4hours. Before statin treatment, cells were transfected with siRNA KLF2 or KLF4.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

4 Samples

Download data: CEL

(Submitter supplied) MEF2C is one of the substantially expressed transcriptional factors in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for MEF2C, and performed ChIP-seq to identify MEF2C binding site in whole genome manner. H3K27Ac binding sites were also detected in the same way.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

3 Samples

Download data: BED, WIG

(Submitter supplied) 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, statins, are known to exert endothelial athero-protective effects through the induction of specific transcriptional factors and their downstream target genes besides lowering LDL-cholesterol. However its critical mechanism has not still been elucidated. Here we report the comprehensive change of transcripts induced by pitavastatin. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4-hours, we identified a group of consistently up - or down - regulated genes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

18 Samples

Download data: CEL