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Endothelial dysfunction in NR2F2-silenced cells - human coronary artery endothelial cells model

ABSTRACT: Endothelial dysfunction in NR2F2-silenced cells - human coronary artery endothelial cells model

PROVIDER: PRJNA779017 | ENA |

REPOSITORIES: ENA

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Endothelial dysfunction in NR2F2-silenced cells - human coronary artery endothelial 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.

2023-05-31 | GSE188466 | GEO

Geometric control of the coronary artery endothelial cell transcriptome following standard growth condition

Project description:Analysis of the effects of cell shape on human coronary artery endothelial cell transcription. The hypothesis is that defined alterations in endothelial cell shape uniquely affect the endothelial transcriptome. Human coronary artery endothelial cells were plated onto spatially defined micropatterns (Cytoo) forcing them to conform to Disc, Crossbow, H, Y, or L shapes. As a control, human coronary artery endothelial cells were plated on non-restrictive areas of the Cytoo growth plate. RNA was collected after 24 hours growth on the restricted or non-restricted growth patterns and subjected to whole genome microarray analysis.

2013-06-01 | E-GEOD-43349 | biostudies-arrayexpress

Geometric control of the coronary artery endothelial cell transcriptome following serum starvation

Project description:Analysis of the effects of cell shape on human coronary artery endothelial cell transcription. The hypothesis is that defined alterations in endothelial cell shape uniquely affect the endothelial transcriptome. Human coronary artery endothelial cells were plated onto spatially defined micropatterns (Cytoo) forcing them to conform to Disc, Crossbow, H, Y, or L shapes. As a control, human coronary artery endothelial cells were plated on non-restrictive areas of the Cytoo growth plate. Cells were serum starved for 48 hours prior to mRNA collection. RNA was collected after 48 hours growth on the restricted or non-restricted growth patterns and subjected to whole genome microarray analysis.

2013-06-01 | E-GEOD-44167 | biostudies-arrayexpress

Geometric control of the coronary artery endothelial cell transcriptome following serum starvation

Project description:Analysis of the effects of cell shape on human coronary artery endothelial cell transcription. The hypothesis is that defined alterations in endothelial cell shape uniquely affect the endothelial transcriptome. Human coronary artery endothelial cells were plated onto spatially defined micropatterns (Cytoo) forcing them to conform to Disc, Crossbow, H, Y, or L shapes. As a control, human coronary artery endothelial cells were plated on non-restrictive areas of the Cytoo growth plate. Cells were serum starved for 48 hours prior to mRNA collection.

2013-06-01 | GSE44167 | GEO

Geometric control of the coronary artery endothelial cell transcriptome following standard growth condition

2013-06-01 | GSE43349 | GEO

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

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

| PRJNA779018 | ENA

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

2023-05-31 | GSE188465 | GEO

Endothelial dysfunction in NR2F2-silenced cells - human lung microvascular endothelial cells model

2023-05-31 | GSE188467 | GEO

Physiological profile of the coronary artery and internal thoracic artery endothelial cells as a basis for the structural and functional congrunce of the arterio-arterial continuum

Project description:Currently, it is well established that human endothelial cells (ECs) are characterised by a significant heterogeneity between distinct blood vessels, e.g., arteries, veins, capillaries, and lymphatic vessels. Further, even ECs belonging to the same lineage but grown under different flow patterns (e.g., laminar and oscillatory or turbulent flow) ostensibly have distinct molecular profiles defining their physiological behaviour. Human coronary artery endothelial cells (HCAEC) and human internal thoracic artery endothelial cells (HITAEC) represent two cell lines inhabiting atheroprone and atheroresistant blood vessels (coronary artery and internal thoracic artery, respectively). Resistance of the internal mammary artery to atherosclerosis has been largely attributed to the protective phenotype of HITAEC which reportedly produce higher amounts of vasodilators including nitric oxide (NO) through the respective signaling pathways. However, this hypothesis has not been adequately addressed hitherto as proteomic profiling of HCAEC and HITAEC in a head-to-head comparison setting has not been performed.

2023-10-17 | PXD037861 | Pride

Endothelial dysfunction in NR2F2-silenced cells - human lung microvascular endothelial cells model

Project description:Endothelial dysfunction in NR2F2-silenced cells - human lung microvascular endothelial cells model

| PRJNA779016 | ENA