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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137580 | GEO | 2020/09/22

REPOSITORIES: GEO

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

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 | GSE137578 | GEO

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 (HAEC miRNA)

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

| PRJNA565964 | ENA

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)

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

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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

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

2010-12-30 | GSE26295 | GEO

Atlas of miRNome variations in different dyslipidemic conditions: a study in C57Bl/6, Ldlr-KO, and Pcsk9-KO mice.

Project description:In this study, mice with different genotypes and fed diets with different lipid content were enrolled, aiming to set up an atlas of miRNA expression levels in different organs with a relevant role in lipid/lipoprotein metabolism. Specifically, three genotypes were investigated: C57Bl/6 mice as controls, together with mice knock-out (KO) for LDLr (low-density lipoprotein receptor) and for PCSK9 (proprotein convertase subtilisin/kexin type 9). LDLr and PCSK9 are both involved in LDL turnover, the former mediating LDL clearance [PMID: 19299327], the latter causing the degradation of the LDLr protein [PMID: 17080197]. As a result, LDLrKO mice, because of their impaired LDL catabolism, are hypercholesterolemic and prone to atherosclerosis development, particularly when fed high-fat, cholesterol-containing diets [PMID: 8349823; PMID: 8182121]. On the contrary, PCSK9KO mice, characterized by an accelerated LDL catabolism, are hypocholesterolemic and atherosclerosis resistant [PMID: 15805190]. miRNA expression was investigated in liver, intestine, aorta, white adipose tissue and brain of mice on both standard and Western diet.

2023-09-06 | GSE227578 | GEO

Effects of intermittent and chronic hypoxia on HAEC

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

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