Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA317739 | ENA |
REPOSITORIES: ENA
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Project description:Intermittent hypoxia (IH) in HeLa cell culture activates proinflammatory transcription factor NFκB, whereas chronic hypoxia (CH) does not. In order to determine whether IH may be linked to vascular inflammation, we developed a novel IH cell culture system and exposed HAEC (human aortic endothelial cells) to IH or CH. Keywords: Human Artery Endothelial Cells (HAEC)
2008-12-31 | GSE10723 | GEO
Project description:While much progress has been made in identifying the mechanisms that trigger endothelial activation and inflammatory cell recruitment during atherosclerosis, less is known about the intrinsic pathways that counteract these events. Here we identified NOTCH1 as an antagonist of endothelial cell activation. NOTCH1 was constitutively expressed by adult arterial endothelium, but levels were significantly reduced by high fat diet. Furthermore, treatment of human aortic endothelial cells (HAEC) with inflammatory lipids (Ox-PAPC) and pro-inflammatory cytokines (TNFalpha and IL1beta) decreased Notch1 expression and signaling in vitro through a mechanism that requires STAT3 activation. Reduction of NOTCH1 in HAEC by siRNA, in the absence of inflammatory lipids or cytokines, increased inflammatory molecules and binding of monocytes. Conversely, some of the effects mediated by Ox-PAPC were reversed by increased NOTCH1 signaling; suggesting a link between lipid-mediated inflammation and Notch1. Interestingly, reduction of NOTCH1 by Ox-PAPC in HAEC was associated with a genetic variant previously correlated to HDL in a human GWAS. Finally endothelial Notch1 heterozygous mice showed higher diet-induced atherosclerosis. Based on these findings, we propose that reduction of endothelial NOTCH1 is a predisposing factor in the onset of vascular inflammation and initiation of atherosclerosis. Transcript profile from Human Aortic Endothelial Cells (HAEC) transfected with siRNA targeting NOTCH1 (n=3) or treated with Ox-PAPC (Oxidized 1-Palmitoyl-2-Arachidonoyl-sn-glycero-3-PhosphoCholine) for 6 hours (n=3) were compared to control HAEC (transfected with control siRNA and control media; n=3).
2015-10-26 | E-GEOD-72633 | biostudies-arrayexpress
Project description:Fidelity of TNF-alpha induced differential gene expression in amplified aRNA samples relative to unamplified RNA samples (human aortic endothelial cells, HAEC).
2005-08-19 | E-CBIL-3 | biostudies-arrayexpress
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
Project description:The effects of 3OC12-HSL on global gene expression in primary human aortic endothelial cells (HAEC).
| PRJNA135057 | ENA
Project description:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison
2005-06-28 | GSE2838 | GEO
Project description:To characterize the transcriptome of primary vascular endothelial cells (ECs) during TNFα-response, we performed total RNA-seq on primary human aortic ECs (HAEC), before and after TNFα (45 min. 10 ng/mL).
2020-06-01 | E-MTAB-7896 | biostudies-arrayexpress
Project description:Cultures of human aortic (HAEC) and pulmonary artery endothelial cells (HPAEC) were exposured to short-term chronic hypoxia (1% O2) for either 0h, 8h or 24h Keywords: Time course, cell-type comparison The response of each cell type (HAEC and HPAEC) to short-term chronic hypoxia was determined by a single SAGE library for each of three time points (0h, 8h and 24h)
2005-06-28 | E-GEOD-2838 | biostudies-arrayexpress
Project description:Analysis of the effect of a bacterial quorum sensing molecule on in-vitro culture of human endothelial cells at gene expression levels. Objective: Chronic infection has long been postulated as a stimulus for atherogenesis. Pseudomonas aeruginosa infection has been associated with increased atherosclerosis in rats, and the bacteria produce a quorum sensing molecule 3-oxo-dodecynoyl-homoserine lactone (3OC12-HSL) that is critical for colonization and virulence. Paraoxonase 2 (PON2) hydrolyzes 3OC12-HSL and also protects against the effects of oxidized phospholipids thought to contribute to atherosclerosis. We now report the response of human aortic endothelial cells (HAEC) to 3OC12-HSL and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC) in relation to PON2 expression. Methods and Results: Using expression profiling and network modeling, we identified the unfolded protein response (UPR), cell cycle genes, and the MAPK signaling pathway to be heavily involved in the HAEC response to 3OC12-HSL. The network also showed striking similarities to a network created based on HAEC response to Ox-PAPC, a major component of minimally-modified LDL. HAEC in which PON2 was silenced by siRNA showed increased pro-inflammatory and UPR responses when treated with 3OC12-HSL or Ox-PAPC. Conclusion: 3OC12-HSL and Ox-PAPC influence similar inflammatory pathways. Quorum sensing molecules such as 3OC12-HSL contribute to the pro-atherogenic effects of chronic infection and the anti-atherogenic effects of PON2 include destruction of quorum sensing molecules. 4 HAEC lines from different donors were treated with 3-O-C12 HSL or control (medium).
2010-12-30 | E-GEOD-26295 | biostudies-arrayexpress
Project description:While much progress has been made in identifying the mechanisms that trigger endothelial activation and inflammatory cell recruitment during atherosclerosis, less is known about the intrinsic pathways that counteract these events. Here we identified NOTCH1 as an antagonist of endothelial cell activation. NOTCH1 was constitutively expressed by adult arterial endothelium, but levels were significantly reduced by high fat diet. Furthermore, treatment of human aortic endothelial cells (HAEC) with inflammatory lipids (Ox-PAPC) and pro-inflammatory cytokines (TNFalpha and IL1beta) decreased Notch1 expression and signaling in vitro through a mechanism that requires STAT3 activation. Reduction of NOTCH1 in HAEC by siRNA, in the absence of inflammatory lipids or cytokines, increased inflammatory molecules and binding of monocytes. Conversely, some of the effects mediated by Ox-PAPC were reversed by increased NOTCH1 signaling; suggesting a link between lipid-mediated inflammation and Notch1. Interestingly, reduction of NOTCH1 by Ox-PAPC in HAEC was associated with a genetic variant previously correlated to HDL in a human GWAS. Finally endothelial Notch1 heterozygous mice showed higher diet-induced atherosclerosis. Based on these findings, we propose that reduction of endothelial NOTCH1 is a predisposing factor in the onset of vascular inflammation and initiation of atherosclerosis.
2015-10-26 | GSE72633 | GEO