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
Project description:The human LncRNA microarray analysis of the 6 monocytes samples from Coronary Artery Disease patients and non Coronary Artery Disease
Project description:Upon activation, platelets release a host of soluble and vesicular signals, collectively termed the ‘platelet releasate’ (PR). The contents of this PR play a significant role in haemostasis, inflammation, and pathologic sequelae. Despite this, proteomic studies investigating the PR in coronary artery disease have not been performed. We undertook a comparative label-free quantitative (LFQ) proteomic profiling of the 1U/ml thrombin-induced PR from 13 acute coronary syndrome (ACS-STEMI) versus 14 stable angina pectoris patients using a tandem mass spectrometry approach. We identified differentially released platet proteins including tetranectin (CLEC3B), protein disulfide-isomerase-A3 (PDIA3), coagulation factor V (F5) and fibronectin (FN1). Strikingly, all 9 differential proteins were associated with the GO cellular component term ‘extracellular vesicle’ and reduced levels of EVs were detected in plasma of ACS-STEMI patients. Network analysis revealed 3 PR proteins either reduced (F5; FN1) or absent (CLEC3B) in ACS-STEMI patients, which are strongly connected to both the clotting cascade and major druggable targets on platelets. This moderated signature highlights the possible basis of platelet dysfunction in ACS-STEMI and may prove useful for non-invasive risk assessment of the progression of coronary artery disease.
Project description:We aimed to clarify the possible functional role of hsa_circ_0000563 in coronary artery disease. Therefore, the ChIRP-MS was conducted to explore the interaction between BTBD7_hsa_circ_0000563 and proteins on a genomic scale in human peripheral blood mononuclear cell (PBMC). This project is the raw files of the proteins bound to hsa_circ_0000563 found by ChIRP-MS in PBMC.
Project description:The identification of classic risk factors for coronary artery disease unveiled pathophysiologic mechanisms of atherosclerosis. Among them, inflammation as a systemic process measurable in peripheral blood plays a central role in plaque progression. However, other mechanisms of plaque progression remain to be fully understood. Therefore, this study sought to further investigate systemic correlates of plaque progression by global gene expression in peripheral blood. Microrarray gene expression analysis revealed 93 genes differentially expressed between the groups, of which 23 genes have no known function. Among the remaining 70 genes, 10 (14%) were identified to be associated with progenitor and pluripotent cells whereas only 3 genes (4%) had been associated with atherosclerosis. A risk prediction gene signature was developed by a multivariable statistical approach model integrating comprehensive laboratory and clinical patient data. This signature identified plaque progression with 81% sensitivity and 80% specificity (AUC: 0.86) for new patients, as estimated by resampling techniques. Array results were validated by qPCR for the genes ankyrin-2 (ANK2) and glutathione S-transferase theta 1 (GSTT1). In conclusion, patients with pogressive coronary artery disease despite good risk factor control exhibit particular gene expression patterns in peripheral blood. Understanding the functional implications of the observed changes might help to design new approaches to control atherosclerosis progression. From a large database of 45,727 coronary angiograms, peripheral blood was drawn from two patient groups with good risk factor control, but different clinical evolution: First, 16 patients with significant lesion progression leading to repeated coronary interventions and second, 16 patients with angiographically documented stable courses.
Project description:Background. In experimental setting the concept of myocardial preconditioning-by hyperoxia has been introduced and different intracellular protective mechanisms and their effects have been described. To study whether similar protective phenotype can be induced by hyperoxia also in humans, gene expression profile after hyperoxic exposure was analyzed. Methods and Findings. Adult patients were randomized to be ventilated with either FiO2 0.4 (n=14) or 1.0 (n=10) for 60 minutes before coronary artery bypass grafting. A tissue sample from the right atrial appendage was taken for gene analysis and expression profile analysis on genome wide level by gene chip analysis was applied. Exposure to > 96% oxygen for 60 minutes significantly changed the expression of 20 different genes, including upregulation of two different humanins - MTRNR2L2 and MTRNR2L8, and activated a “cell survival” network as detected by Ingenuity Pathway Analyses. Conclusions. Administration of > 96% oxygen for 1 hour changes gene expression in the myocardium of the patients with coronary artery disease and may enhance cell survival capability. Background. In experimental setting the concept of myocardial preconditioning-by hyperoxia has been introduced and different intracellular protective mechanisms and their effects have been described. To study whether similar protective phenotype can be induced by hyperoxia also in humans, gene expression profile after hyperoxic exposure was analyzed. Methods and Findings. Adult patients were randomized to be ventilated with either FiO2 0.4 (n=14) or 1.0 (n=10) for 60 minutes before coronary artery bypass grafting. A tissue sample from the right atrial appendage was taken for gene analysis and expression profile analysis on genome wide level by gene chip analysis was applied. Exposure to > 96% oxygen for 60 minutes significantly changed the expression of 20 different genes, including upregulation of two different humanins - MTRNR2L2 and MTRNR2L8, and activated a “cell survival” network as detected by Ingenuity Pathway Analyses. Conclusions. Administration of > 96% oxygen for 1 hour changes gene expression in the myocardium of the patients with coronary artery disease and may enhance cell survival capability. 24 samples, 14 controls and 10 with intervention