Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The expression profile in EA.hy926 cells after exposure to hypoxic conditions was evaluated by RNA-sequencing.

ABSTRACT: Hypoxia is an imbalance between oxygen supply and demand that occurs in embryonic development, as well as in pathological situations such as cancer, ischemic heart disease, and wound healing. To cope with decreased oxygen concentrations, a series of biological processes that endothelial cells participate in such as angiogenesis, are transcriptionally activated. In this work, we performed RNA-sequencing to profile activated genes in EA.hy926 cells after 8 hours of hypoxia, to reveal the changes of gene expression profile in endothelial cells under hypoxia.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176365 | GEO | 2021/06/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

Project description:Endothelial dysfunction in NR2F2-silenced cells - EA.hy926 cells model

| PRJNA779018 | ENA

Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

Project description:As the climate changes due to global warming, the frequency of appearance of marine-derived toxins increases. In particular, the need to investigate marine-derived toxins for which toxicity has not yet been identified is emerging. Blood vessels are passageways through which compounds entering the body move to various organs and are the sites first exposed to compounds. Therefore, it is important to know the effects of compounds on blood vessels when they enter the body. In this study, the human vascular endothelial cell line EA.hy926 was exposed to the marine toxins OA (IC20; 42.9 nM) and the mechanism of toxicity was investigated at the transcriptome level. Quantseq 3' mRNA sequencing was performed by extracting RNA from EA.hy926 cells exposed to the toxins. Differentially expressed genes were determined based on fold change ≥ 1.5 and P value < 0.05.

2024-05-18 | GSE267374 | GEO

The expression profile in EA.hy926 cells after exposure to hypoxic conditions was evaluated by RNA-sequencing.

Project description:The expression profile in EA.hy926 cells after exposure to hypoxic conditions was evaluated by RNA-sequencing.

| PRJNA736024 | ENA

Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

Project description:Transcriptomic analysis of human vascular endothelial cell line (EA.hy926) exposed to okadaic acid

| PRJNA1111366 | ENA

Impact of Nfat5 on normoxia- and hypoxia-exposed mouse lung endothelial cells

Project description:Chronic hypoxia causes detrimental structural alterations in the lung, which are partially dependent on stress responses of the endothelium. In this context, we revealed that hypoxia-exposed murine lung endothelial cells (MLEC) activate nuclear factor of activated T-cells 5 (NFAT5/TonEBP) - a transcription factor that adjusts the cellular transcriptome to cope with multiple environmental stressors. Here, we studied the impact of NFAT5 on hypoxia-induced gene expression in MLEC by comparing the transcriptome of control and Nfat5-deficient MLEC, which were isolated from mouse lungs after exposure to normoxia and hypoxia for 7 days and processed for scRNA seq.

2024-08-08 | GSE255681 | GEO

Analysis of transcriptome in normoxia/hypoxia(21d)-exposed lungs upon KO of Nfat5 in ECs

Project description:Chronic hypoxic stress stimulates lung endothelial cells to promote vascular remodeling processes, which - in the long run - increase the resistance of pulmonary arteries. While several molecular determinants promoting these maladaptive changes have been delineated, their transcriptional regulation is not well studied. In this context, we revealed that hypoxia activates nuclear factor of activated T-cells 5 (NFAT5/TonEBP) in murine lung endothelial cells (MLECs) - a transcription factor that regulates the adjustment of the cellular transcriptome to cope with osmotic, biomechanical or metabolic environmental stressors. Here, we studied the functional relevance of NFAT5 for the control of endothelial hypoxic stress responses in the lung. Genetic ablation of Nfat5 in endothelial cells did not evoke any obvious phenotypic alterations under normoxia. However, microarray-based transcriptome analyses of lung tissue revealed significant alterations 7 but not 21 days after exposure to normobaric hypoxia (10% O2).

2024-08-08 | GSE230053 | GEO

Analysis of transcriptome in hypoxia(7d)-exposed lungs upon KO of Nfat5 in ECs

2024-08-08 | GSE230052 | GEO

Individual nucleotide resolution Crosslinking Immunoprecipitation (iCLIP)-seq

Project description:Purpose: to identify the AGO1-bound miRNAs and mRNAs in human endothelial cells subject to hypoxic condition (2% oxygen) Methods: human microvascular endothelial cells was cultured under normoxia (20% oxygen) or hypoxia (2%) oxygen for 24 hours. Total RNA was extracted and RNA and small RNA libraries were prepared for Seq. Results: We found substantial changes in AGO1-bound mRNAs due to hypoxia. A portion of CLIP-seq reads also reveal direct binding to miRNA to mRNA. Conclusions: hypoxia induces profound changes in mRNAs associated with AGO1.

2019-09-06 | GSE136907 | GEO

Characterization of two distinct immortalized endothelial cell lines HMEC-1 and EA.hy926 for in vitro studies: exploring the impact of calcium electroporation, Ca2+ signaling and transcriptome profile

Project description:The vascular endothelium consists of endothelial cells (ECs) with important biological functions and their impairment is associated with various pathologies. ECs vary based on tissue origin and gene expression, while their functionality depends on calcium (Ca2+) signaling. In tumors, disruption of Ca2+ homeostasis after calcium electroporation (CaEP) has been shown to elicit an enhanced antitumor effect with only minimal effect on normal tissue. The difference in response to CaEP was not only observed between cancer and normal cells, but also between different endothelial cell lines. Although several vascular EC models have been developed, there is a lack of understanding regarding the molecular basis that could help explain different responses of normal tissue to CaEP. Therefore, our study aims to determine the effect of CaEP on established immortalized human EC lines EA.hy926 and HMEC-1 in terms of cytoskeleton, Ca2+ kinetics and differences in gene expression involved in regulation of Ca2+ signaling and homeostasis.

2024-02-21 | GSE244042 | GEO

Resting natural killer cell homeostasis relies on tryptophan/NAD+ metabolism and HIF-1α

Project description:Natural killer (NK) cells are forced to cope with different oxygen environments even under resting conditions. The adaptation to low oxygen is regulated by oxygen-sensitive transcription factors, the hypoxia-inducible factors (HIFs). The function of HIFs for NK cell activation and metabolic rewiring remains controversial. Activated NK cells are predominantly glycolytic, but the metabolic programs that ensure the maintenance of resting NK cells are enigmatic. By combining in situ metabolomic and transcriptomic analyses in resting murine NK cells, our study defines HIF-1a as a regulator of tryptophan metabolism and cellular nicotinamide adenine dinucleotide (NAD+) levels. The HIF-1a/NAD+ axis prevents ROS production during oxidative phosphorylation (OxPhos) and thereby blocks DNA damage and NK cell apoptosis under steadystate conditions. In contrast, in activated NK cells under hypoxia, HIF-1a is required for glycolysis, and forced HIF-1a expression boosts glycolysis and NK cell performance in vitro and in vivo. Our data highlight two distinct pathways by which HIF-1a interferes with NK cell metabolism. While HIF-1a-driven glycolysis is essential for NK cell activation, resting NK cell homeostasis relies on HIF-1a-dependent tryptophan/NAD+ metabolism. Linked cross omic data sets:RNA-seq data associated with this study are available in ArrayExpress (BioStudies): accession <a href='https://www.ebi.ac.uk/biostudies/arrayexpress/studies/E-MTAB-12082' rel='noopener noreferrer' target='_blank'>E-MTAB-12082</a>.

2023-06-01 | MTBLS6863 | MetaboLights

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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