Transcriptomic profiles of human aortic smooth muscle cell (HASMC) which exposed to M(con) or M(Hb) macrophage supernatant with osteogenic conponents supplementation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE222453 | GEO | 2023/01/10
REPOSITORIES: GEO
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Project description:Plaque rupture and subsequent thrombus formation is responsible for the majority of clinical complications of atherosclerosis and nonetheless our understanding of what underlies plaque vulnerability and rupture is still sparse and mostly deductively based on animal models and in vitro studies. We adopted five different -omics platforms to compare ruptured atherosclerotic and advanced-stable tissue within the same carotid plaque specimen from 24 carotid endarterectomy patients. Segments designated as stable feature either a fibrous cap atheroma or pathological intimal thickening. Segments designated as ruptured include a thrombus and/or presented intraplaque hemorrhage. For the present study only those samples were selected for further analysis that were flanked by two segments of identical classification, be it stable (S) or ruptured (R); and were derived from CEA specimen that contained plaque segments of both classifications.
2014-05-17 | E-MTAB-2055 | biostudies-arrayexpress
Project description:Transcriptional profiling of stable and unstable atherosclerotic plaque segments from human carotid endatrerectomies Objective Comparison of gene expression in stable versus unstable atherosclerotic plaque may be confounded by interpatient variability. The aim of this study was to identify differences in gene expression between stable and unstable segments of plaque obtained from the same patient. Human carotid endarterectomy specimens were segmented and macroscopically classified using a morphological classification system. Two analytical methods, an intraplaque and an interplaque analysis, revealed 170 and 1916 differentially expressed genes, respectively using Affymetrix gene chip analysis. A total of 115 genes were identified from both analyses. The differential expression of 27 genes was also confirmed using quantitative-polymerase chain reaction on a larger panel of samples. Eighteen of these genes have not been associated previously with plaque instability, including the metalloproteinase, ADAMDEC1 (37-fold), retinoic acid receptor responder-1 (5-fold), and cysteine protease legumain (3-fold). Matrix metalloproteinase-9 (MMP-9), cathepsin B, and a novel gene, legumain, a potential activator of MMPs and cathepsins, were also confirmed at the protein level. The differential expression of 18 genes not previously associated with plaque rupture has been confirmed in stable and unstable regions of the same atherosclerotic plaque. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability. Differential gene expression in stable and unstable plaque was assessed by whole transcriptome analysis. Intraplaque analysis by QT-PCR confirmed the differential expression of 18 genes not associated previously with plaque rupture. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability
2006-01-30 | E-TABM-190 | biostudies-arrayexpress
Project description:Atherosclerosis is a lipid-driven inflammatory disease.However, evidence emerging so far from single cell atlases suggests a dichotomy between lipid associated and inflammatory macrophage states. Here, we present the most inclusive reference atlas of human intraplaque immune cell communities to date.
2023-05-22 | GSE210152 | GEO
Project description:Atherosclerosis is the leading underlying cause of death worldwide. We reported a mouse model of atherosclerosis regression that involves transplanting an atherosclerotic aortic arch into a normolipidemic mouse. There, emigration of plaque foam cells occurred in a CCR7 (dendritic cell migration factor) dependent manner. It was obvious, though, that other pathways are likely to be involved in this process. We therefore performed microarrays on laser captured macrophages isolated from the progression and regression environments. This yielded two major findings. Firstly, genes associated with the contractile apparatus (such as actin and myosin) that are responsible for cellular movement were differentially up-regulated under regression conditions with members of the cadherin family (serves in adhesion functions) being significantly down-regulated. Secondly, the most highly up-regulated gene under regression was arginase I, a classical marker of the M2 alternative activated macrophage. Further examination revealed that regression was characterized by macrophages displaying other M2 markers such as CD163, C-lectin receptor, mannose receptor, and Fizz-1. In addition, we applied recently introduced local causal pathway discovery methods to our microarray data that revealed that genes such as vinculin and ApoCII may play a role in the pathophysiology of atherosclerosis regression. Ultimately, the insights gained from the regression model and the different modes of analyses should lead to new therapeutic targets against cardiovascular disease. We performed microarrays on laser captured macrophages isolated from aortic arch from mouse in atherosclerosis progression and regression environments (C57Bl/6, ApoE -/-). Study was performed in two batches, with three treatment groups each: progression, regression and baseline. Profiled in the Merck/Agilent 3.0
2011-09-30 | E-GEOD-24819 | biostudies-arrayexpress
Project description:Neutrophil extracellular traps (NETs) promote inflammation and atherosclerosis progression. In diabetes they are increased and impair wound healing, during which inflammation normally resolves. Atherosclerosis regression, a process resembling wound healing, is also impaired in diabetes. Thus, we hypothesized that NETs impede atherosclerosis regression in diabetes through unresolved inflammation. Objective: To investigate in diabetes the effect of NETs on plaque macrophage inflammation and whether NETs reduction improves atherosclerosis regression. Findings: Transcriptomic profiling of plaque macrophages from NET positive and negative areas in Ldlr-/- mice revealed inflammasome and glycolysis pathway upregulation, indicating a pro-inflammatory phenotype. During atherosclerosis regression in non-diabetic mice, plaque NET content decreased. In contrast, in diabetic mouse plaques NETs were enriched and persisted after lipid-lowering. DNase1 treatment (to degrade NETs) of diabetic mice reduced plaque NETs and macrophage inflammation and improved atherosclerosis regression after lipid-lowering. Conclusions: NETs decline during atherosclerosis regression in non-diabetic mice, but persist in diabetes and impair regression by exacerbating macrophage inflammation. DNase1 reduced diabetic plaque NETs and macrophage inflammation, and restored atherosclerosis resolution after lipid-lowering, despite ongoing hyperglycemia. Given that humans with diabetes also exhibit impaired atherosclerosis resolution with lipid-lowering, these data suggest that NETs contribute to the increased CVD risk in this population.
2020-05-12 | GSE145200 | GEO
Project description:Low frequency Jak2VF mutations promote atherosclerosis via IL-1 mediated cross-talk. Therapeutic approaches that increase MERTK or TREM2 could promote plaque stabilization in inflammasome-driven atherosclerosis.
2024-11-26 | GSE280703 | GEO
Project description:Background: Somatic mutations in blood indicative of clonal hematopoiesis of indeterminate potential (CHIP), particularly in DNMT3A, TET2, and JAK2, are associated with an increased risk of hematologic malignancy, coronary artery disease, and all-cause mortality. However, whether CHIP is associated with increased risk of peripheral artery disease (PAD) remains unknown. In addition, chemotherapy frequently causes mutations in DNA Damage Repair (DDR) genes TP53 and PPM1D, and whether CHIP caused by somatic mutations in DDR genes results in increased risk of atherosclerosis is unclear. We sought to test whether CHIP, and CHIP caused by DDR genes, associates with incident peripheral artery disease (PAD) and atherosclerosis. Methods: We identified CHIP among 50,122 exome sequences in individuals from UK and Mass General Brigham Biobanks and tested CHIP status (N=2,851) with incident PAD and atherosclerosis across multiple arterial beds. To mimic the human scenario of clonal hematopoiesis and test whether the expansion of p53-deficient hematopoietic cells contributes to atherosclerosis, a competitive bone marrow transplantation (BMT) strategy was used to generate atherosclerosis-prone Ldlr-/- chimeric mice carrying 20% Trp53-/- hematopoietic cells (20% KO-BMT mice). We then evaluated aortic plaque burden and plaque macrophage accumulation 12 weeks after grafting. Results: CHIP associated with incident PAD (HR 1.7; P=2.2x10-5) and atherosclerosis in multiple beds (HR 1.3; P=9.7x10-5), with increased risk among individuals with DDR CHIP (HR 2.0; P=0.0084). Among atherosclerosis-prone Ldlr null mice, the p53 -/- 20% KO-BMT mice demonstrated increased aortic plaque size (p=0.013) and accumulation of p53-/- plaque macrophages (P<0.001), driven by an abundance of p53-deficient plaque macrophages. The expansion of p53-deficient cells did not affect the expression of the pro-inflammatory cytokines IL-6 and IL-1β in the atherosclerotic aortic wall. Conclusions: Our findings highlight the role of CHIP as a broad driver of atherosclerosis across the entire arterial system, with evidence of increased plaque among p53 -/- 20% KO-BMT mice via expansion of plaque macrophages. These observations provide new insight into the link between CHIP and cardiovascular disease, and lend human genetic support to the concept that post-cytotoxic chemotherapy patients may benefit from surveillance for atherosclerotic conditions in addition to therapy-related myeloid neoplasms.
2022-11-29 | GSE184420 | GEO
Project description:The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression.
2022-07-20 | GSE203523 | GEO
Project description:The rupture of atherosclerotic plaque contributes significantly to cardiovascular disease (CVD). Plasma concentrations of bilirubin, a by-product of heme catabolism, inversely associate with risk of CVD, although the link between bilirubin and atherosclerosis remains unclear.
2024-02-22 | PXD040314 | JPOST Repository