Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA109569 | ENA |
REPOSITORIES: ENA
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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
Project description:The goal of this study was to profile transcriptional changes of mouse peritoneal macrophages during foam cell formation induced by the atherogenic lipoprotein, oxidized LDL (oxLDL)
2014-12-04 | GSE58913 | GEO
Project description:Oxidized LDL induce macrophages to turn into foam cells in a CD36 dependent manner. The Goal of this study is to compare transcriptome profile by RNA-seq among WT/CD36 knockout macrophages treated with or without oxLDL. We detected re-organization of lipid metabolisms as well as immune activation by oxLDL.
2019-10-28 | GSE139439 | GEO
Project description:Oxidized low-density lipoprotein (oxLDL) is a known risk factor for atherogenesis. However, it is not clear what are the key components of oxLDL driving atherosclerosis.This study aimed to reveal structural features of oxLDL present in circulation of patients with acute myocardial infarction (AMI) and healthy subjects. Total LDL and HDL were separated from pooled sera prepared from 3-6 indivisuals of 25 AMI patients and plasma of seven healthy subjects using ultracentrifugation.When LDL was fractionated on an anion-exchange column, in vivo-oxLDL of AMI patients and healthy subjects, detected by the anti-oxidized phosphatidylcholine (oxPC) monoclonal antibody, was concentrated in electronegative LDL (LDL(-)) fraction. Surprisingly, LDL(-) fraction contained HDL-sized particles in addition to LDL observed using transmission electron microscopy. LC-MS/MS revealed this fraction contaned oxidized apolipoprotein A1 (apoA1) and all lysine residues of the oxidized apoA1 were modified by acrolein. The electronegative in vivo-oxLDL was immunologically purified from the LDL(-) fraction with an anti-oxPC monoclonal antibody, and LC-MS/MS analysis carried out to explore oxidatively modified peptides; but only a small number of acrolein-modified residues identified in the apoB. We propose that oxidized HDL interacts with in vivo-oxLDL that is involved in atherosclerosis.
2020-03-10 | PXD017957 | JPOST Repository
Project description:The transition of the endothelium to a pro-inflammatory state is key to progression of chronic inflammatory diseases including rheumatoid arthritis, chronic bowel disease and atherosclerosis. In atherosclerosis it is hypothesized that low density lipoproteins (LDL) that become trapped in the intima of the blood vessels are oxidized to minimally modified LDL (mmLDL) and that these serve as an important contributing factors to endothelial dysfunction. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphatidylcholine (OX-PAPC), a model of the active phospholipid components of mmLDL affects the expression of hundreds of genes involved in inflammatory and other biological processes in human aortic endothelial cells (HAECs). We hypothesized that microRNAs (miRNAs) partially regulate this response. Using next generation sequencing, we identified miR-21-3p and miR-27a-5p to be induced 4-fold and 3-fold, respectively in response to OX-PAPC treatment compared to control treatment in HAECs. To identify the targets, we performed whole genome transcript profiling following transient over-expression of these two miRNAs followed by. In total, 1254 genes were down-regulated with 925 of them overlapping between the two miRNAs. Functional enrichment analysis using Gene Ontology predicted that the two miRNAs were involved in the regulation of NF-κB signaling. We characterized the Toll/interleukin-1 receptor (TIR) domain-containing adaptor protein TICAM2 as a direct target of miR-21-3p and miR-27a-5p. Furthermore, we showed that over-expression of miR-21-3p and miR-27a-5p lead to decreased p65 translocation to the nucleus and decreased the expression of known NF-κB downstream target genes confirming both miRNAs’ role in negatively regulating NF-κB signaling in endothelial cells. mRNA expression profiling of human aortic endothelial cells from two separate donors that were transfected with 1 nM microRNA mimics and negative control. The miRIDIAN mimics used were miR-21-3p (Catalog Number:C-301023-01-0005), miR-27a-5p (Catalog No: C-301028-01-0005), negative control (Catalog No: CN-001000-01-05)
2014-06-01 | E-GEOD-48006 | biostudies-arrayexpress
Project description:The liver is the central organ for cholesterol synthesis and homeostasis. The effects of dietary cholesterol on hepatic injury, mainly of oxidized low-density lipoproteins (OxLDL), are not fully understood. Here, we show that the degree of cholesterol oxidation had different impacts on the global gene expression of human M2-like macrophages, with highly oxidized LDL causing the most dramatic changes. M2-like macrophages and Kupffer cells undergo M4-like polarization, decreasing the expression of important markers, such as IL10, MRC1, and CD163. These cells also displayed functional changes, with reduced phagocytic capacity, increased neutrophil recruitment, and more effective neutrophil extracellular traps (NETs) induction. Our findings provide a link between the accumulation of OxLDL and NASH progression, offering a new target for NAFLD treatment.
2021-05-25 | GSE160200 | GEO
Project description:Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) are important regulators of immune responses and promoters of tumor progression in cancer1,2. The heterogeneity of these cells as well as their distinction from neutrophils hampers the progress in understanding of the biology and clinical significance of these cells. PMN-MDSC had a distinct gene signature from neutrophils isolated from the same patients with most prominent changes in genes associated with endoplasmic reticulum (ER) stress response. Surprisingly, low-density lipoprotein (LDL) was one of the most enriched gene regulators and oxidized LDL receptor 1 (OLR1) was one of the most overexpressed genes in PMN-MDSC. Lectin-type oxidized LDL receptor 1 (LOX-1) encoded by OLR1 was expressed in only 0.7% of neutrophils in peripheral blood of healthy donors, whereas 5-15% of neutrophils in cancer patients and 15-50% of neutrophils in tumor tissues were LOX-1+. In contrast to their LOX-1- counterparts, LOX-1+ neutrophils had gene signature, biochemical and functional characteristics of PMN-MDSC. Induction of ER stress in neutrophils from healthy donors up-regulated LOX-1 expression and converted these cells to suppressive PMN-MDSC. Thus, PMN-MDSC have distinct gene signature and LOX-1 can define this population of cells, which may provide new insight to the biology and clinical evaluation of these cells. Examination of LOX1+/LOX1- and PMN/MDSC cells in cancer patient samples
2016-07-22 | E-GEOD-79404 | biostudies-arrayexpress
Project description:The aim of the experiment was to determine the effects of 48 hours of treatment with oxidized low density lipoprotein (oxLDL) on gene expression in primary human monocyte-derived macrophages. 6 independent biological replicates were processed. From each replicate half of the cells were treated with oxLDL and the other half were treated with the control buffer. For foam cell formation (after 7 days) macrophages were treated with oxLDL (50mcg/ml, enodtoxin free, Copper oxidized). Control macrophages were treated with a matching buffer without oxLDL. Treatment duration - 48 hours.
2015-04-08 | E-GEOD-54666 | biostudies-arrayexpress
Project description:Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) are important regulators of immune responses and promoters of tumor progression in cancer1,2. The heterogeneity of these cells as well as their distinction from neutrophils hampers the progress in understanding of the biology and clinical significance of these cells. PMN-MDSC had a distinct gene signature from neutrophils isolated from the same patients with most prominent changes in genes associated with endoplasmic reticulum (ER) stress response. Surprisingly, low-density lipoprotein (LDL) was one of the most enriched gene regulators and oxidized LDL receptor 1 (OLR1) was one of the most overexpressed genes in PMN-MDSC. Lectin-type oxidized LDL receptor 1 (LOX-1) encoded by OLR1 was expressed in only 0.7% of neutrophils in peripheral blood of healthy donors, whereas 5-15% of neutrophils in cancer patients and 15-50% of neutrophils in tumor tissues were LOX-1+. In contrast to their LOX-1- counterparts, LOX-1+ neutrophils had gene signature, biochemical and functional characteristics of PMN-MDSC. Induction of ER stress in neutrophils from healthy donors up-regulated LOX-1 expression and converted these cells to suppressive PMN-MDSC. Thus, PMN-MDSC have distinct gene signature and LOX-1 can define this population of cells, which may provide new insight to the biology and clinical evaluation of these cells.
2016-07-22 | GSE79404 | GEO
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