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Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

ABSTRACT: Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

PROVIDER: PRJNA565964 | ENA |

REPOSITORIES: ENA

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Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

Project description:Atherosclerosis (AS), which is a chronic inflammatory disease, is the leading cause of death worldwide. Although several miRNAs have been reported to participate in regulating the progression of AS, there is a lack of systematic study of miRNA profile in AS. We combined miRNA and mRNA array analysis to study the global miRNAs in two AS models-oxidative LDL treated human aortic endothelial cells (HAEC) and high fat diet fed ldlr W483Stop knockin mouse. Novel miRNAs were identified to function in AS through inflammation and apoptosis pathways.

2020-09-22 | GSE137580 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

2020-09-22 | GSE137578 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

| PRJNA565963 | ENA

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

2020-09-22 | GSE137582 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

2020-09-22 | GSE137581 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

| PRJNA565966 | ENA

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

| PRJNA565965 | ENA

Microbiota HAEC

Project description:Microbiota HAEC

| PRJEB55092 | ENA

Endothelial NOTCH1 is suppressed by circulating lipids and antagonizes inflammation during atherosclerosis

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

The effects of 3OC12-HSL on global gene expression in primary human aortic endothelial cells (HAEC).

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

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