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Transcriptome analysis of human aortic valvular endothelial cells with PPARG knockdown and oxLDL treatment.

ABSTRACT: Transcriptome analysis of human aortic valvular endothelial cells with PPARG knockdown and oxLDL treatment.

PROVIDER: PRJNA852779 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19850470_1.fastq.gz	Fastqsanger.gz
	SRR19850470_2.fastq.gz	Fastqsanger.gz
	SRR19850471_1.fastq.gz	Fastqsanger.gz
	SRR19850471_2.fastq.gz	Fastqsanger.gz
	SRR19850472_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of human aortic valvular endothelial cells with PPARG knockdown and oxLDL treatment.

Project description:We isolated and cultured human aortic valvular endothelial cells from patients, and performed RNA sequencing of human aortic valvular endothelial cells transfected with siRNA targeting PPARG or negative control siRNA and treated with or without oxLDL.

2022-08-22 | GSE206927 | GEO

Discovery of Shear- and Side-specific mRNAs and miRNAs in Human Aortic Valvular Endothelial Cells

Project description:Identify shear and side-specific miRNAs in Human Aortic Valvular Endothelial Cells using the following conditions: 1) fHAVEC exposed to OS (FO), 2) vHAVEC exposed to OS (VO), 3) fHAVEC exposed to LS (FL), and 4) vHAVEC exposed to LS (VL).

2011-11-29 | GSE26953 | GEO

Discovery of Shear- and Side-specific mRNAs and miRNAs in Human Aortic Valvular Endothelial Cells

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Protein profiling of Aortic-Valvular and Endocardial endothelial cells using label-free proteomics

Project description:The variations in the protein profile of aortic-valvular (AVE) and endocardial endothelial (EE) cells are currently unknown. The current study's objective is to identify differentially expressed proteins and associated pathways in both endothelial cells. We used endothelial cells isolated from the porcine aortic valve and endocardium for the profiling of proteins. Label-free proteomics was performed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Our proteomics analysis revealed that 29 proteins were highly expressed, and 25 proteins were less represented in the valve than endocardial endothelium. The first part of the study was already available in the ProteomeXchange Consortium (PXD009194).

2022-02-17 | PXD025922 | Pride

Transcriptome analysis of valvular interstitial cells (VICs) treated with lipoprotein (LDL or oxLDL)

Project description:Transcriptome analysis of valvular interstitial cells (VICs) treated with lipoprotein (LDL or oxLDL)

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Exploring molecular profiles of calcification in aortic vascular smooth muscle cells and aortic valvular interstitial cells

Project description:Cardiovascular calcification can occur in vascular and valvular structures and is commonly associated with calcium deposition and tissue mineralization leading to stiffness and dysfunction. Based on shared risk factors and end stage pathologies, calcific aortic valve disease (CAVD) and coronary artery calcification (CAC) are often considered as one disease, and similarly treated. However, the clinical conditions associated with each phenotype can be different, suggesting multifaceted pathologies. To better understand diversity in molecular and cellular processes that underlie calcification in vascular and valvular structures, we exposed aortic vascular smooth muscle cells (AVSMCs) and aortic valve interstitial cells (AVICs) to calcific stimuli including high (2.5mM) phosphate and osteogenic media (OM) treatments in vitro. Consistent with clinical observations made by others, we show that AVSMCs are more susceptible to calcification than AVICs, and this process is mediated by cell-specific and treatment-specific molecular responses. RNA-seq analysis demonstrates that in response to calcific-stimuli, both AVSMCs and AVICs activate a robust ossification-program, although the signaling pathways, cellular processes and osteogenic-associated markers involved are diverse. In addition, VIC-mediated calcification appears to involve biological processes related to osteo-chondro differentiation and down regulation of actin cytoskeleton genes, that are not observed in VSMCs. Furthermore, are findings suggest that signaling pathways involved in cardiovascular cell calcification are dependent on the calcific-stimuli, including a requirement of PI3K signaling for OM-induced calcification, and not 2.5mM Phosphate. Together, this study provides a wealth of information suggesting that the pathogenesis of cardiovascular calcifications may be significantly more diverse than previously appreciated.

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Exploring molecular profiles of osteogenically differentiated aortic valvular interstitial cells

Project description:Exploring molecular profiles of osteogenically differentiated aortic valvular interstitial cells

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LOX-1-dependent transcriptional regulation after oxidized LDL (OxLDL) treatment of human aortic endothelial cells.

Project description:LOX-1 is the primary endothelial receptor for oxidized LDL in endothelial cells and plays a role in the development of atherosclerosis. Expression profiling was carried out on samples from HAECT cells over-expressing either LOX-1 or GFP control and treated with or without OxLDL over a time course of 2, 6, 12 and 24 Hours. The goal of the study was to identify genes expression changes activated by OxLDL binding to LOX-1 at several different time points.

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Metabolomics Characterization of Human Calcific Aortic Valve Stenosis

Project description:BACKGROUND: Calcific aortic valve stenosis (CAVS) is the most prevalent valvular heart disease in developed countries with significant morbidity and mortality. Given the poor understanding of the pathophysiological processes leading to CAVS, we utilized a joint non-targeted metabolomics and targeted lipidomics approach to better characterize the metabolic perturbations involved in its development and progression.METHODS: We collected human aortic valve tissue from 106 patients undergoing aortic valve replacement surgery. Our cohort represented aortic valvular hemodynamics from mild to severe aortic stenosis with varying degrees of valvular calcification.RESULTS: Seventy-two significantly differential (p<0.01) metabolites across different stages of CAVS severity were filtered and identified from the tissue metabolome. Each stage of valvular stenosis was characterized by a distinct metabolic signature. The top three perturbed metabolic pathways in the setting of CAVS involved glycerophospholipid metabolism, linoleic acid metabolism and primary bile acid biosynthesis. The lysophosphatidic acid species (LysoPA) exhibited significant (p<0.05) association with CAVS severity and were also found to select patients with accelerated rate of CAVS progression. Two LysoPA species namely, 18:2 LysoPA and 20:4 LysoPA, exhibited potential to serve as biomarkers of CAVS severity.CONCLUSIONS: The present study reports the largest and most comprehensive metabolomics analysis of human aortic valve stenosis that highlights the dysregulated LysoPA pathway involved in the pathogenesis of CAVS.

2020-02-03 | MTBLS1267 | MetaboLights

Transcriptome analysis of valvular interstitial cells (VICs) treated with lipoprotein (LDL or oxLDL)

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