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Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

ABSTRACT: Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

PROVIDER: PRJNA579159 | ENA |

REPOSITORIES: ENA

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Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

Project description:We have employed transcriptome microarray expression profiling as a discovery platform to figure out the pharmacological mechanisms of quercetin against endothelial senescence induced by ox-LDL in vitro. Expression of RCHY1, EIF4E1B, IGFBP3, SERPINE1, BRAF, SLC5A11 from this signature was quantified in the same kind of samples by real-time PCR, confirming the change pattern.

2019-10-29 | GSE139288 | GEO

Quercetin Attenuates Atherosclerosis via Modulating Oxidized LDL-Induced Endothelial Cellular Senescence.

Project description:Background and Aims:Endothelial senescence is an important risk factor leading to atherosclerosis. The mechanism of quercetin against endothelial senescence is worth exploring. Methods:Quercetin (20 mg/kg/d) was administered to ApoE-/- mice intragastrically to evaluate the effectiveness of quercetin on atherosclerotic lesion in vivo. In vitro, human aortic endothelial cells (HAECs) were used to assess the effect of quercetin on cellular senescence induced by oxidized low-density lipoprotein (ox-LDL). Transcriptome microarray and quantitative RT-PCR was conducted to study the pharmacological targets of quercetin. Results:ApoE-/- mice demonstrated obvious lipid deposition in arterial lumina, high level of serum sIcam-1 and IL-6, and high density of Vcam-1 and lower density of Sirt1 in aorta. Quercetin administration decreased lipid deposition in arterial lumina, serum sIcam-1, and IL-6 and Vcam-1 in aorta, while increased the density of Sirt1 in aorta of ApoE-/- mice. In vitro, quercetin (0.3, 1, or 3 ?mol/L) decreased the expression of senescence-associated ?-galactosidase and improved cell morphology of HAECs. And quercetin decreased the cellular apoptosis and increased mitochondrial membrane potential (??m) in dose-dependent manner, and decreased ROS generation simultaneously. Transcriptome microarray suggested 254 differentially expressed (DE) mRNAs (110 mRNAs were upregulated and 144 mRNAs were downregulated) in HAECs after quercetin treatment (fold change > 1.5, P?< 0?.05, Que vs Ox-LDL). GO and KEGG analysis indicated nitrogen metabolism, ECM-receptor interaction, complement, and coagulation cascades, p53 and mTOR signaling pathway were involved in the pharmacological mechanisms of quercetin against ox-LDL. Conclusions:Quercetin alleviated atherosclerotic lesion both in vivo and in vitro.

| S-EPMC7198817 | biostudies-literature

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.

2009-10-07 | GSE13139 | GEO

Radiation Impacts Early Atherosclerosis by Suppressing Intimal LDL Accumulation

Project description:We report that bone marrow transplantation suppresses atherosclerosis by reducing LDL accumulation in the intima. Radiation exposure enhances endothelial endolysosomal trafficking and cholesterol efflux pathways, thus preventing reducing the abundance of LDL particles that traverse the endothelial layer to deposit in the sub-endothelial space.

2021-03-31 | GSE163206 | GEO

Expression data from human vascular smooth muscle cells exposed to minimally oxidized (mox) LDL

Project description:Atherosclerosis (AT) is a chronic inflammatory disease characterized by the accumulation of inflammatory cells, lipoproteins and fibrous tissue in the walls of arteries. AT is the primary cause of heart attacks and stroke and the leading cause of death in westernized countries. To date, the pathogenesis of AT is not well-defined. Studies have shown that the dedifferentiation of contractile and quiescent vascular smooth muscle cells (SMC) to the proliferative, migratory and synthetic phenotype in the intima is pivotal for the onset and progression of AT. To further delineate the mechanisms underlying the pathogenesis of AT, we have analyzed the early molecular pathways and networks of SMC phenotype transformation as induced by the presence of minimally-oxidized LDL (moxLDL). 3 pooled samples were analyzed, one untreated control, one 3h after treatment, one 21h after treatment, no replicates

2012-03-16 | E-GEOD-36487 | biostudies-arrayexpress

Effect of MKP5 deletion in bone-marrow-derived macrophages on gene expression during oxidized-LDL stimulation

Project description:MKP-5 is a MAP kinase phosphatase that is responsible for the dephosphorylation of MAP kinases p-38 MAPK, JNK, and sometimes ERK. MKP-5 has been implicated in many diseases and its deletion results in increased inflammation. However, MKP-5 expression and regulation have not been studied in atherosclerosis, and our project aims to identify MKP-5 as a relevant gene in this disease. Specifically, we aim to identify the role of MKP-5 in the regulation of plaque stability. In atherosclerotic diseased states, oxidized LDL particles promote inflammatory mechanisms and form macrophage foam cells. We show that comparing wild-type and MKP-5-/- bone-marrow-derived macrophages stimulated with oxidized-LDL, results in the identification of significant gene expressions and major up- and down-regulated targeted pathways via bulk-RNA sequencing. Taken together, our data provides an unbiased way to test the mechanistic role of MKP-5 in an atherogenic environment. Furthermore, our data confirms and contributes to the current knowledge of gene expression influenced by MKP-5, as well as the influence of MKP-5 deletion on pathways critical to plaque stability including inflammation and collagen synthesis and deposition.

2024-02-12 | GSE251637 | GEO

Expression data from human vascular smooth muscle cells exposed to minimally oxidized (mox) LDL

2012-03-16 | GSE36487 | GEO

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [miRNA-Seq]

Project description:High-throughput Sequencing has revolutionized system-based analysis of cellular pathways. The goals of this study are to find the effect of quercetin pretreatment on the transcriptome of ox-LDL injured endothelial cells

2024-02-24 | GSE167392 | GEO

High-throughput Sequencing Facilitates Quantitative Analysis of Transcriptome Difference Underlying Quercetin Antioxidant Action in Ox-LDL-induced HUVECs Damage [ncRNA-Seq]

2024-02-24 | GSE167391 | GEO

Transcription profiling of human monocyte derived macrophages from atherosclerosis subjects vs. controls

Project description:The project was designed to identify genes with an altered expression in macrophages from subjects with atherosclerosis compared to macrophages from control subjects. Experiment Overall Design: We used monocyte-derived macrophages from peripheral blood cultured in the absence or presence of oxidized LDL, baseline macrophages or foam cells. The macrophages were obtained from 15 subjects with subclinical atherosclerosis and a family history of CHD. Macrophages from 15 age and sexmatched subjects with no atherosclerosis and no family history of CHD were used as control.

2008-06-17 | E-GEOD-9874 | biostudies-arrayexpress

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