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Circulating miRNA profile and coronary calcification in asymptomatic patients with familial hypercholesterolemia.

ABSTRACT: Circulating miRNA profile and coronary calcification in asymptomatic patients with familial hypercholesterolemia.

PROVIDER: PRJNA737428 | ENA |

REPOSITORIES: ENA

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Circulating miRNA profile and coronary calcification in asymptomatic patients with familial hypercholesterolemia.

Project description:Affymetrix microarray (GeneChip microRNA 4.0) profilling of circulating miRNAs. We used miRNA arrays to profile miRNAs isolated from plasma from familial hypercholesterolemia patients with (FH-W_CCS) or without (FH-WO_CCS) coronary calcium score by computed tomographic angiography

2024-03-26 | GSE178126 | GEO

Insulin-like growth factor I reduces coronary atherosclerosis in pigs with familial hypercholesterolemia

Project description:To investigate effects of IGF-1 on human-like coronary atherosclerosis we used high fat diet-fed Rapacz pigs with familial hypercholesterolemia (FH pigs). We used spatial transcriptomics (ST) analysis to identify global transcriptome changes in advanced plaque compartments and to obtain mechanistic insights into IGF-1 effects. IGF-1-injected FH pigs had 1.8-fold increase in total circulating IGF-1 levels compared to control. IGF-1 decreased relative coronary atheroma (data obtained by serial intravascular ultrasound) and lesion cross-sectional area (post-mortem histology). IGF-1 increased fibrous cap thickness, and reduced necrotic core size, macrophage content, and cell apoptosis, changes consistent with promotion of a stable plaque phenotype. ST analysis revealed that IGF-1 suppressed FOS/FOSB factors and gene expression of MMP9 and CXCL14 suggesting possible involvement of these molecules in IGF-1’s effect on atherosclerosis.

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Atherosclerotic markers in human blood - a study in patients with familial hypercholesterolemia

Project description:Atherosclerosis is characterized by thickening of the arterial wall and is the primary cause of the coronary artery disease and cerebrovascular disease, two of the most common causes of illness and death worldwide. One of the leading risk factors for development of atherosclerosis is familial hypercholesterolemia. Familial hypercholesterolemia is an autosomal dominant disorder, which is caused by mutations mainly located in the low-density lipoprotein receptor (LDLR) gene. It is characterized by elevated levels of low-density lipoprotein cholesterol, the presence of tendon xanthomas, and premature cardiovascular disease. Aim of this study was to find atherosclerotic markers in white blood cells of patients compared to healthy controls. None of these patients exhibited symptoms of atherosclerosis by standard diagnostic methods; however, transcriptome analysis of blood RNA indicated changes in ubiquitin proteolysis and cell adhesion system as expected in initiation steps of atherosclerosis.

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Transcription profiling by array of human familial hypercholesterolemia to identify atherosclerotic markers in human blood

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Project description:Insulin-like growth factor I reduces coronary atherosclerosis in pigs with familial hypercholesterolemia

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Project description:Atherosclerosis is a chronic disease involving multiple biological mechanisms. A study aimed to identify changes in miRNA expression at early stages using a large swine model. 18 female pigs were studied, 9 with familial hypercholesterolemia and 9 normal controls. Plasma was collected at 3, 6, and 9 months of age. In vivo imaging and histopathology were performed to document the presence of coronary atherosclerosis. miRNA sequencing was carried out on plasma cell-free RNA. Results showed that circulating miRNA dynamics change over time during atherosclerosis development and specific DE miRNAs may be promising biomarkers for early detection of coronary atherosclerosis.

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Integrative DNA, RNA and protein evidence connects TREML4 to coronary artery calcification

Project description:Peripheral blood RNA-Seq from human coronary artery calcification cases and controls; Coronary artery calcification (CAC) is a heritable and definitive morphologic marker of atherosclerosis that strongly predicts risk for future cardiovascular events. To search for genes involved in CAC, we used an integrative transcriptomic, genomic, and protein expression strategy using next-generation DNA sequencing in the discovery phase with follow-up studies using traditional molecular biology and histopathology techniques. Eight cases and eight controls (matched for gender, age and ancestry); RNA sequencing of peripheral blood from a discovery set of eight CAC cases and eight matched controls was used to identify dysregulated genes, which were validated using the NanoString® and Affymetrix GeneChip® Human Exon ST Array platforms. The median CAC scores for cases in the screening and validation sets were 1531.5 and 668.5, respectively, while all controls had a score of zero.

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Imprints of atherosclerosis are present in circulating T cells of patients with Familial Hypercholesterolemia

Project description:Atherosclerosis is the major cause of death in industrialized countries. This disease has initially been characterized as a lipid disorder, but current concepts argue for an inflammatory disease, which develops in the background of hypercholesterolemia and other risk factors. In response to initial events of atherosclerosis formation, such as LDL-deposition in the subendothelial space, monocytes and T cells interact with the vessel wall. However, little is known about the properties and the behavior of these cells in this context. Using familial hypercholesterolemia (FH) as a model we demonstrate substantial differences in the gene expression of freshly isolated human monocytes and T lymphocytes. In FH monocytes we found an increased uptake of oxidized LDL, elevated amounts of scavenger receptors and adhesion molecules, and differences in the regulation of intracellular lipoprotein metabolism compared to monocytes from healthy individuals. Furthermore, the monocyte subpopulation of CD14+/CD16+ cells is less frequent in FH but exhibits significantly higher levels of CD11c and CD29 which increases the likelihood for their transmigration through the endothelial layer. The presence of increased amounts of CD69 in T lymphocytes from FH patients suggests that these cells are more activated than control cells. Our results indicate that some important steps of atherosclerosis formation already take place in circulating blood cells which extends current atherosclerosis models to the plasma compartment. Keywords: atherosclerosis, T cells, Familial Hypercholesterolemia

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