Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction
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ABSTRACT:
PROVIDER: PRJNA1120858 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29309478_1.fastq.gz | Fastqsanger.gz | |||
| SRR29309478_2.fastq.gz | Fastqsanger.gz | |||
| SRR29309479_1.fastq.gz | Fastqsanger.gz | |||
| SRR29309479_2.fastq.gz | Fastqsanger.gz | |||
| SRR29309480_1.fastq.gz | Fastqsanger.gz |
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Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.
2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress
Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work
2014-10-23 | GSE62646 | GEO
Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs)
2013-11-15 | GSE47495 | GEO
Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.
2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress
Project description:There is an unmet need to develop new strategies to improve risk stratification in patients with myocardial infarction and to identify new targets for intervention. The aim of this study was to establish the unbiased peripheral blood whole transcriptome response in myocardial infarction, and to correlate it with clinical characteristics and outcome. RNA expression was determined in the acute phase of MI and at follow-up, and related to clinical phenotype and outcome.
2019-11-24 | GSE123342 | GEO
Project description:We studied new microRNAs involved in the left ventricular adverse remodeling (LVAR) process after the ST elevation myocardial infarction (STEMI). We analyzed the expression of miRNAs in peripheral blood mononuclear cells (PBMCs) isolated from a group of non-LVAR (n = 5) and LVAR STEMI patients (n = 5), before (0 hour) and after a primary percutaneous coronary intervention (PPCI; 6 hours).
2022-03-11 | E-MTAB-11002 | biostudies-arrayexpress
Project description:Background: Acute myocardial infarction (AMI) can occur in patients with atherosclerotic disease, with or without plaque rupture. Previous studies have indicated a set of immune responses to plaque rupture. However, the specific circulating immune cell subsets that mediate inflammatory plaque rupture remain elusive. Methods: Ten AMI patients were enrolled in our study (five with and five without plaque rupture; plaque characteristics were identified by optical coherence tomography). By single-cell RNA sequencing, we analyzed the transcriptomic profile of peripheral blood mononuclear cells. Results: We identified 27 cell clusters among 82,550 cells, including monocytes, T cells, NK cells, B cells, megakaryocytes, and CD34+ cells. Classical and non-classical monocytes constitute the major inflammatory cell types, and pro-inflammatory genes such as CCL5, TLR7, and CX3CR1 were significantly upregulated in patients with plaque rupture, while the neutrophil activation and degranulation genes FPR2, MMP9, and CLEC4D were significantly expressed in the intermediate monocytes derived from patients without plaque rupture. We also found that CD4+ effector T cells may contribute to plaque rupture by producing a range of cytokines and inflammatory_x0002_related chemokines, while CD8+ effector T cells express more effector molecules in patients without plaque rupture, such as GZMB, GNLY, and PRF1, which may contribute to the progress of plaque erosion. Additionally, NK and B cells played a significant role in activating inflammatory cells and promoting chemokine production in the plaque rupture. Cell?cell communication elaborated characteristics in signaling pathways dominated by inflammatory activation of classical monocytes in patients with plaque rupture. Conclusions: Our studies demonstrate that the circulating immune cells of patients with plaque rupture exhibit highly pro-inflammatory characteristics, while plaque erosion is mainly associated with intermediate monocyte amplification, neutrophil activation, and degranulation. These findings may provide novel targets for the precise treatment of patients with AMI.
2024-06-12 | GSE269269 | GEO
Project description:Analysis of peripheral blood specimens from patients with acute myocardial infarction (AMI). Results provide insight into molecular mechanisms associated with AMI.
2018-12-08 | GSE123487 | GEO
Project description:Peripheral blood mononuclear cell hyperresponsiveness in patients with premature myocardial infarction without traditional risk factors
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Project description:An increasing number of patients develop a myocardial infarction (MI) in the absence of standard modifiable risk factors (SMuRFs). Atherosclerosis is characterized by a chronic arterial wall inflammation in which monocyte-derived macrophages play a pivotal role. Trained immunity – a long lasting hyperreactive state of innate immune cells – might contribute to the development of atherosclerosis. This study investigated whether trained immunity is observed in this specific patient group. 20 SMuRFless MI patients who suffered an atherothrombotic myocardial infarction > 1 year and < 4 years before inclusion were recruited. All patients were younger than 50 years of age during the index event. Patients were matched to 18 healthy controls without coronary atherosclerosis as determined by a coronary CT-scan. Blood samples were obtained two weeks after interrupting statins in patients and starting aspirin therapy in controls to match relevant medication use. Circulating inflammatory parameters and monocytes were analyzed, with an in-depth focus on peripheral blood mononuclear cell (PBMC) function, and monocyte phenotype, RNA expression and epigenetic histone markers. PBMCs from SMuRFless patients showed higher cytokine production upon ex vivo stimulation. Although baseline RNA expression and monocyte activations markers were largely unchanged, enrichment of the transcriptionally permissive histone marker H3K4me3 on the promoter region of cytokine genes was observedIL-10 genes was observed. This existed without differences in systemic inflammation. Circulating monocytes in young SMuRFless MI patients have a hyperresponsive functional and epigenetic phenotype, indicative of trained immunity. In the absence of traditional risk factors, this could be a promising target for future therapy in these patients.
2023-07-19 | GSE229044 | GEO