Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Clustering of Surrogates of Cardiovascular Risk Factors Results in Emergent Phenotypes in Endothelial Cells

ABSTRACT: Global gene expression of human coronary artery endothelial cells (HCAEC) submitted surrogates of cardiovascular risk factors Based on the analysis of global gene expression in human coronary artery endothelial cells (HCAEC), we identified gene pathways and inferred cellular processes that are modulated in response to chemical hypoxia, oxidized lipids, IL-1β and oscillatory flow or combined stimuli. Our results indicate that clustering of the surrogates of risk factors is different from the sum of the individual insults that give rise to emergent phenotypes such as cell proliferation. Altogether, we provide evidence of a hierarchical effect between risk factor surrogates and advent of emergent phenotypes in response to combined stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181822 | GEO | 2022/02/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Clustering of Surrogates of Cardiovascular Risk Factors Results in Emergent Phenotypes in Endothelial Cells

Project description:Clustering of Surrogates of Cardiovascular Risk Factors Results in Emergent Phenotypes in Endothelial Cells

| PRJNA753527 | ENA

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

Human vascular endothelial cells display different gene expression patterns and response to EGF

Project description:RNA sequencing was performed for human primary aortic (HAoEC) and coronary artery (HCAEC) endothelial cells from female donors, after incubation with or without EGF.

2023-12-27 | GSE206410 | GEO

Expression profiling of Endothelial (EC) and Non-endothelial Cells

Project description:Gene expression profiling of HUVEC (human umbilical vein EC cell; Lonza), HAEC (human aortic EC cells), HCAEC (human coronary artery EC cells), HPAEC (human pulmonary artery EC cells), HMVEC (human microvascular (dermal) , HASMC ( Human Aortic Smooth Muscle Cells), T cells and Bcells. Gene expression profiling of Endothelial cells and Non-endothelial cells in order to identify the genes with preferntial expression to endothelial cells. The experiments are performed in duplicate on both the HT Human Genome U133A and U133B arrays.

2011-04-04 | E-GEOD-21212 | biostudies-arrayexpress

Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C

Project description:Genotoxic stress in mammalian cells defined as a situation that initiates DNA damage compromising the cell’s genomic integrity leading to replication and transcription arrest underlies many pathological conditions including cellular senescence, cancer and cardiovascular diseases. Recent experimental data suggest that genotoxic stress in vitro induced by alkylating mutagen mitomycin C (MMC) is associated with proinflammatory activation of primary human endothelial cells and endothelial-to-mesenchymal transition, the key pathways underlying endothelial disfunction – an initial stage of atherosclerosis, a leading cause of cardiovascular morbidity and mortality worldwide. Given the increasing genotoxic load on the human organism from various environmental (ionizing and UV radiation) and anthropogenic (tobacco smoke, exhaust gases, industrial waste) sources, the decryption of molecular pathways underlying genotoxic stress induced endothelial dysfunction could improve our understanding of atherogenesis and help to justification of genotoxic stress as a novel risk factor for atherosclerosis. Therefore, we performed label-free proteomic profiling of Commercially available primary human coronary artery endothelial cells (HCAEC) and ) and internal thoracic artery endothelial cells (HITAEC) in vitro exposed to MMC followed by bioinformatic analysis to identify biochemical pathways and functional proteins underlying genotoxic stress induced endothelial dysfunction.

2024-06-22 | PXD050743 | Pride

Exploration of gene expression signature for human coronary artery endothelial cells in response to inhibition of myocyte enhancer factor 2A

Project description:Myocyte enhancer factor 2A (MEF2A) is a crucial transcritional activator which plays diverse roles in the control of cell growth, survival, apoptosis and inflammation etc. To expore the gene expression signature of human coronary artery endothelial cells (HCAEC) in reponse to inhibition of MEF2A， we have employed whole genome microarray expression profiling as a discovery platform to identify genes with important functional role in HCAEC. Three independent groups of HCAEC transfected with MEF2A specific siRNA were separately performed. Three MEF2A specific siRNA groups were indicated as 1527-1, 1527-2 and 1527-3, and the mixed control group was designated as NC.

2019-01-01 | GSE114114 | GEO

Global gene expression profile of human peripheral blood-derived endothelial colony-forming cells is similar to coronary artery and umbilical vein endothelial cells

Project description:We performed a transcriptome-wide study to compare gene expression profiles of ECFC, human coronary artery endothelial cells (HCAEC) and human umbilical vein endothelial cells (HUVEC) utilising subcutaneous adipose tissue-derived stromal vascular fraction (SAT-SVF) as a negative control population. Baseline gene expression in ECFC fully corresponds to their endothelial specification and may contribute to the basement membrane organisation, fulfilling the requirements for the suitable cell population for in vitro pre-endothelialisation of tubular scaffolds.

2019-05-31 | GSE131995 | GEO

Expression profiling of Endothelial (EC) and Non-endothelial Cells

2011-04-04 | GSE21212 | GEO

Endothelial Cells from different anatomical origin have distinct responses during Snail/TGF-β2-mediated Endothelial-Mesenchymal Transition

Project description:Endothelial-mesenchymal transition (EndMT) is a complex process, in which differentiated endothelial cells undergo phenotypic transition to mesenchymal cells. Given the diversity of the vascular system in architecture, structure, and embryonic origins, it is not clear if endothelial cells lining different vessels are able to undergo EndMT. Therefore, the aim of this study was to evaluate the molecular and functional changes that occur in different types of endothelial cells after induction of EndMT through overexpression of Snail and TGF-β2. Different types of endothelial cells (human umbilical vein, heart, and lung) have distinct response when induced to undergo EndMT. Coronary artery endothelial cells (HCAEC) induced with combined Snail overexpression plus TGF-β2 treatment promotes a decrease of endothelial markers, an increase of mesenchymal markers and migration. The mechanism that HCAEC undergoing EndMT may be mediated through Notch and non-canonical Wnt signaling pathways. These results provide the foundation for understanding the roles of specific signaling pathways in mediating EndMT in endothelial cells from different anatomical origin.

2017-04-22 | GSE96089 | GEO

Gene expression profile of endothelial cell cultures exposed to uremic serum from Chronic Kidney Disease patients: role of MAPK signaling pathway

Project description:Transcriptome analysis of human coronary arterial endothelial cells (HCAEC) primary cultures exposed to uremic serum from patients with stage 4-5 cardiovascular diseases (CKD) without myocardial infarction (USI) and stage 4-5 CKD with myocardial infarction (UCI). Gene expression profile of human coronary arterial endothelial cells (HCAEC) primary cultures exposed to uremic serum from of patients with chronic kidney disease (CKD) that explore which pathways are involved in in the development of cardiovascular disease. The metabolic pathway significantly represented was the MAPK signaling pathway, suggesting that the effects of uremic toxins present in patients with CDK, on the primary cultures of HCAEC provides a more informative model for the study of molecular mechanisms that lead to the development of endothelial dysfunction secondary to CKD.

2019-01-31 | GSE125898 | GEO

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