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

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

PROVIDER: PRJNA1111366 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29015846.fastq.gz	Fastqsanger.gz
	SRR29015847.fastq.gz	Fastqsanger.gz
	SRR29015848.fastq.gz	Fastqsanger.gz
	SRR29015849.fastq.gz	Fastqsanger.gz
	SRR29015850.fastq.gz	Fastqsanger.gz

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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

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

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Argopecten irradians, gills, exposed to okadaic acid

Project description:Differential expression analysis of gill tissues of bay scallop (Argopecten irradians) exposed to okadaic acid at a concentration of 500 nM for 48 h.

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Argopecten irradians, gills, exposed to okadaic acid

Project description:Argopecten irradians, gills, exposed to okadaic acid

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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.

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Regulation of oxidative stress in endothelial cells exposed to high glucose by selected microRNA

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Mytilus galloprovincialis, digestive gland and gill, exposed to Prorocentrum lima, producers of okadaic acid.

Project description:Differential expression analysis of digestive gland and gill tissues of mussels (Mytilus galloprovincialis) exposed to dinoflagellates (Prorocentrum lima), producers of okadaic acid, at a concentration of 200 cells/ml for one day. Each sample consists in total RNA was extracted from pooled tissues of 5 individuals. Two-color dye-swap direct comparison experiment: exposed vs non-exposed (treated vs control). Biological replicates: two treated replicates and two control replicates per tissue.

2015-11-19 | E-GEOD-72817 | biostudies-arrayexpress

Mytilus galloprovincialis, digestive gland and gill, exposed to Prorocentrum lima, producers of okadaic acid.

2015-11-19 | GSE72817 | GEO

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

Project description:Orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor 2 (COUPTF2; NR2F2) is highly expressed in endothelial cells (ECs) and Nr2f2 knockout produces lethal cardiovascular defects. In humans, NR2F2 mutations result in both congenital heart disease and diaphragmatic hernia, conditions associated with the development of pulmonary arterial hypertension (PAH). However, COUPTF2 functions in mature endothelium are uncertain. NR2F2 knockdown in primary human endothelial cells (ECs) led to an interferon-biased inflammatory response, endothelial-to-mesenchymal transition, proliferation, hypermigration, apoptosis-resistance and mitochondrial dysfunction. These phenotypic changes were associated with AKT activation and increased Dickkopf-1 (DKK1) expression, a Wnt/β-catenin pathway inhibitor. DKK1 was also elevated in patients with PAH and secreted in response to loss of bone morphogenetic receptor type 2 (BMPR2), the archetypal PAH-associated genetic defect. Together, these findings demonstrate that endothelial NR2F2 suppresses inflammation and proliferation. Thus, NR2F2 loss disrupts EC homeostasis and may promote pathologic vascular remodeling in the development of PAH.

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

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2021-06-09 | GSE176365 | GEO

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