STAMPEED: Atherosclerotic Disease, Vascular Function, and Genetic Epidemiology (ADVANCE)
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PROVIDER: PRJNA76503 | ENA |
REPOSITORIES: ENA
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Project description:STAMPEED: Atherosclerotic Disease, Vascular Function, and Genetic Epidemiology (ADVANCE)
| PRJNA76505 | ENA
Project description:STAMPEED: Genetic Epidemiology Network of Arteriopathy (GENOA)
| PRJNA75885 | ENA
Project description:<p>ADVANCE (Atherosclerotic Disease, VAscular functioN, and genetiC Epidemiology) is a large epidemiological study of genetic and non-genetic determinants of coronary artery disease (CAD) that started in 2000 as a collaborative effort between researchers at Stanford University and Kaiser Permanente of Northern California. The overarching goal of the study is to improve our ability to prevent, diagnose and treat CAD. The initial study included recruitment of over 3600 subjects (including 1873 subjects with incident clinically significant coronary disease and 1745 control subjects) from multiple race/ethnic backgrounds. A subset of ~ 500 subjects with very early onset coronary disease (men < 45 and women < 55) and ~ 500 similar aged controls were genotyped using the Illumina 550K platform as part of an NIH funded effort within the STAMPEED consortium.</p>
| phs000423.v1.p1 | EGA
Project description:SGLT-2 inhibitors, such as empagliflozin, have been shown to reduce the occurrence of cardiovascular events and delay the progression of atherosclerosis. However, its role in atherosclerotic calcification remains unclear. In this research, ApoE-/- mice were fed with western diet and empagliflozin was added to the drinking water for 24 weeks. Empagliflozin treatment significantly alleviated arterial calcification assessed by alizarin red and von kossa staining in aortic roots and reduced the lipid levels, while had little effect on body weight and blood glucose levels in ApoE-/- mice. In vitro studies, empagliflozin significantly inhibits calcification of primary vascular smooth muscle cells (VSMCs) and aortic rings induced by osteogenic media (OM) or inorganic phosphorus (Pi). RNA sequencing of VSMCs cultured in OM with or without empagliflozin showed that empagliflozin negatively regulated the osteogenic differentiation of VSMCs. And further studies confirmed that empagliflozin significantly inhibited osteogenic differentiation of VSMCs via qRT-PCR. Our study demonstrates that empagliflozin alleviates atherosclerotic calcification by inhibiting osteogenic differentiation of VSMCs, which addressed a critical need for the discovery of a drug-based therapeutic approach in the treatment of atherosclerotic calcification.
2023-11-22 | GSE243752 | GEO
Project description:Vascular calcification is the ectopic deposition of calcium hydroxyapatite minerals in arterial wall. However, the underlying molecular mechanisms regulating vascular calcification remain incompletely understood. In this study, we applied RNA sequencing to explore the mechanism of vascular calcificaiton in both medial and atherosclerotic vascular calcification models.
2021-02-23 | GSE159832 | GEO
Project description:Chaperone-mediated autophagy (CMA) contributes to regulation of energy homeostasis by timely degradation of enzymes involved in glucose and lipid metabolism. Here, we report reduced CMA activity in vascular smooth muscle cells and macrophages in murine and human arteries in response to atherosclerotic challenges. We show that in vivo genetic blockage of CMA worsens atherosclerotic pathology through both systemic and cell-autonomous changes in vascular smooth muscle cells and macrophages, the two main cell types involved in atherogenesis. CMA deficiency promotes dedifferentiation of vascular smooth muscle cells and a pro-inflammatory state in macrophages. Conversely, a genetic mouse model with upregulated CMA shows lower vulnerability to the pro-atherosclerotic challenge. We propose that CMA could be an attractive therapeutic target against cardiovascular diseases.
2022-03-14 | GSE143162 | GEO
Project description:Atherosclerosis leads to vascular lesions that involve major rearrangements of the vascular proteome, especially of the extracellular matrix (ECM). Using single aortas from ApoE knock out mice, we quantified formation of plaques by single-run, high-resolution mass spectrometry (MS)-based proteomics. To probe localization on a proteome-wide scale, we employed quantitative detergent solubility profiling. This compartment- and time-resolved resource of atherogenesis comprised 5,117 proteins, 182 of which changed their expression status in response to vessel maturation and atherosclerotic plaque development. In the insoluble ECM proteome, 65 proteins significantly changed, including relevant collagens, matrix metalloproteinases and macrophage specific proteins.
2017-12-08 | PXD006752 | Pride
Project description:In response to vascular injury, early EPC or Circulating angiogenic cells (CAC) are thought to be recruited to the damaged areas, participating mainly in a paracrine fashion, by releasing pro-angiogenic factors, promoting the mobilization of other cell populations such as the late EPC, or endothelial colony-forming cells (ECFC). ECFC will help by replacing the damaged endothelium and promoting neovascularization. Unfortunately, however, despite the regenerative role, the number and function of EPC are severely affected under pathological conditions, making compulsory to better understand how these cells react under those environments in order to implement their use in regenerative cell therapies. Herein we evaluated, for the first time to our knowledge, the effect of atherosclerotic factors over the paracrine role of CAC, by direct incubation ex vivo of healthy CAC with the secretome of atherosclerotic arteries. The application of a label free proteomics approach allowed the identification of 194 altered proteins in the secretome of pre-conditioned CAC, many of them related, among others, with inhibition of angiogenesis and cell migration. Functional assays corroborated that, after atherosclerotic pre-conditioning, the pro-angiogenic effect of CAC over ECFC was impaired, affecting ECFC migration as well as their ability to form tubules on a basement membrane matrix assay. Up-regulation of several anti-angiogenic proteins in the CAC secretome could help to explain such angiogenic switch which, in turns, could reflect a protective and beneficial effect against the atherosclerotic process.
2021-09-09 | PXD019395 | Pride
Project description:STAMPEED: Myocardial Infarction Genetics Consortium (MIGen)
| PRJNA75665 | ENA