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PROVIDER: PRJNA686838 | ENA |
REPOSITORIES: ENA
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Project description:The human LncRNA microarray analysis of the 6 monocytes samples from Coronary Artery Disease patients and non Coronary Artery Disease 3 Coronary Artery Disease patients and 3 non-Coronary Artery Disease donors
2015-06-05 | E-GEOD-69587 | biostudies-arrayexpress
Project description:The human LncRNA microarray analysis of the 6 monocytes samples from Coronary Artery Disease patients and non Coronary Artery Disease
2015-06-05 | GSE69587 | GEO
Project description:We took samples of subcutaneous adipose tissue from the sternum (SAT) and epicardial adipose tissue (EAT) from a site adjacent to the right coronary artery in cases with coronary disease and controls without coronary disease. Cases had significant coronary disease and were undergoing coronary artery bypass surgery. Controls all had coronary angiograms and did not have significant coronary disease.
2018-10-04 | GSE120774 | GEO
Project description:The human LncRNA microarray analysis of the 6 plasma samples from Coronary Artery Disease patients and non Coronary Artery Disease
2015-05-05 | GSE68506 | GEO
Project description:Background: Kawasaki Disease (KD) is a childhood illness of suspected infectious etiology that causes medium-sized muscular arteritis, most critically affecting the coronary arteries. No single diagnostic test exists, hampering early diagnosis and treatment. Approximately 25% of untreated patients develop coronary artery disease, and children who are treated with intravenous gammaglobulin but do not respond are also at high risk. Subacute/chronic arteritis and luminal myofibroblastic proliferation are the pathologic processes occurring in KD CA after the second week of illness, when neutrophilic necrotizing arteritis has subsided. The specific dysregulated immune pathways contributing to subacute/chronic arteritis have been unknown, hampering the development of effective immunomodulatory therapies for patients not responding to intravenous gammaglobulin therapy. Methods and Results: Deep RNA sequencing was performed on KD (n=8) and childhood control (n=7) coronary artery tissues, revealing 1074 differentially expressed mRNAs. Molecular pathways involving T helper cell, cytotoxic T lymphocyte, dendritic cells, and antigen presentation were the most significantly dysregulated. There was significant upregulation of immunoglobulin and type I interferon-stimulated genes. 80 upregulated extracellular genes encoding secreted proteins are candidate biomarkers of KD arteritis. Conclusions: The immune transcriptional profile in KD coronary artery tissues is primarily T helper and cytotoxic lymphocyte-mediated, and has features of an antiviral immune response such as type I interferon-stimulated gene expression. This first report of the KD coronary artery transcriptome identifies specific dysregulated immune response pathways that can inform the development of new therapies for and biomarkers of KD arteritis, and provide direction for future etiologic studies.
2016-04-22 | GSE64486 | GEO
Project description:Coronary artery disease (CAD) is the leading cause of mortality worldwide. We aimed to compare expression of miRNA in the affected artery of acute myocardial infarction (ST-elevation myocardial infarction) male patients versus healthy individuals (control). Blood samples were collected during coronary catheterization from proximal culprit coronary arteries aimed for the interventions or from a random artery in control samples. RNA isolated from serum was used for miRNA high throughput sequencing.
2023-04-23 | GSE230165 | GEO
Project description:Vascular endothelial cells play an important role in the development of coronary artery disease, their injury leads to coronary heart disease and atherosclerosis. This study aimed to elucidate the role of FOXO3-regulated target gene expression and alternative splicing in vascular endothelial cell injury in coronary artery disease
2024-02-09 | GSE225605 | GEO
Project description:The relation of serial changes in plaque morphology of obstructive nonculprit lesions to HDL efflux, inflammation and transcriptome perturbations in response to high-dose statin therapy (YELLOW II study). YELLOW II is a prospective single center study. Stable patients who were scheduled for elective coronary angiography and/or coronary artery stenting were screened for this study. The final target population were patients with multivessel disease requiring staged intervention, culprit vessel initially and non-culprit vessel later, with maxLCBI4mm greater than 150 by NIRS. Patients underwent PCI for a culprit lesion followed by OCT and NIRS/IVUS of an obstructive non-culprit lesion (NCL). All subjects received rosuvastatin, 40 mg every day for 8-12 weeks. The NCL was reimaged and underwent intervention as a part of staged intervention. Blood samples were obtained for cholesterol efflux capacity (CEC) quantification and peripheral PBMC isolation. Despite the extensive evidence for the beneficial effects of statins on clinical outcomes, the mechanisms underlying these effects in remain elusive. In a prospective study, 85 patients with stable multivessel coronary artery disease underwent percutaneous coronary intervention for a culprit lesion followed by intracoronary multi-modality imaging including optical coherence tomography (OCT) of an obstructive NCL. All subjects received 40 mg of rosuvastatin every day for 8-12 weeks, when the NCL was reimaged and intervention was performed. Blood samples were drawn at both times to assess cholesterol efflux capacity (CEC) and transcriptomic profile in peripheral blood mononuclear cells (PBMC).
2016-10-29 | GSE86216 | GEO
Project description:Mitophagy is a major quality control pathway that removes unwanted or dysfunctional mitochondria, and plays an essential role in vascular health. Here we show that MCM8 expression is significantly decreased in children with Kawasaki disease (KD) who developed coronary artery aneurysms. Mechanistically, we discover that nitric oxide (NO) signaling promotes TRIM21 mediated MCM8 ubiquitination, which disrupts its interaction with MCM9 and promotes its cytosolic export. In the cytosol, MCM8 relocates to the mitochondria pore forming proteins and promotes their ubiquitination by TRIM21. In addition, MCM8 directly recruits LC3 via its LIR motif and initiates mitophagy. This suppresses mitochondrial DNA-mediated activation of type I interferon via cGAS and STING. Mice that are deficient in Mcm8, Trim21, Nos2, or reconstituted with the East-Asian specific MCM8-P276 variant develop more severe coronary artery vasculopathy in the Lactobacillus casei extract-induced KD model. Collectively, the data suggest that MCM8 protects vascular health in the KD setting.
2023-06-29 | GSE235994 | GEO
Project description:Aryl-hydrocarbon receptor protects against endochondral ossification of modulated smooth muscle cells in atherosclerosis Introduction: Smooth muscle cells (SMC) play a critical role in atherosclerosis. The Aryl hydrocarbon receptor (AHR) is an environment-sensing transcription factor that contributes to vascular development, and has been implicated in coronary artery disease (CAD) risk. We hypothesized that AHR can affect atherosclerosis by regulating phenotypic modulation of SMC. Methods: We combined RNA-Seq, ChIP-Seq, ATAC-Seq and in-vitro assays in human coronary artery SMC (HCASMC), with single-cell RNA-Seq (scRNA-Seq), histology, and RNAscope in an SMC-specific lineage-tracing Ahr knockout mouse model of atherosclerosis to better understand the role of AHR in vascular disease. Results: Genomic studies coupled with functional assays in cultured HCASMC revealed that AHR modulates HCASMC phenotype and suppresses ossification in these cells. Lineage tracing and activity tracing studies in the mouse aortic sinus showed that the Ahr pathway is active in modulated SMC in the atherosclerotic lesion cap. Furthermore, scRNA-Seq studies of the SMC-specific Ahr knockout mice showed a significant increase in the proportion of modulated SMC expressing chondrocyte markers such as Col2a1 and Alpl, which localized to the lesion neointima. These cells, which we term chondromyocytes (CMC), were also identified in the neointima of human coronary arteries. In histological analyses, these changes manifested as larger lesion size, increased lineage-traced SMC participation in the lesion, decreased lineage-traced SMC in the lesion cap, and increased alkaline phosphatase activity in lesions in the Ahr knockout compared to wild-type mice. We propose that AHR is likely protective based on these data and inference from human genetic analyses. Conclusion: Overall, we conclude that AHR promotes maintenance of lesion cap integrity and diminishes the disease related SMC-to-CMC transition in atherosclerotic tissues.
2020-07-01 | GSE150768 | GEO