Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pericardial fluid microRNAs in patients with arrhythmogenic right ventricular cardiomyopathy or ischemic heart disease

ABSTRACT: Pericardial fluid is enriched by biologically active molecules of cardiovascular origin including microRNAs. Investigation of the disease-specific extracellular microRNAs could shed light on the molecular processes underlying disease development. Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart disease characterized by life-threatening arrhythmias and progressive heart failure development. The current data about the association between microRNAs and ARVC development are limited. We performed small RNA sequence analysis of microRNAs of pericardial fluid samples obtained during transcutaneous epicardial access for ventricular tachycardia (VT) ablation of six patients with definite ARVC and three post-infarction VT patients. Disease-associated microRNAs of pericardial fluid were identified. Enrichment analysis of differentially expressed microRNAs revealed their close linkage to cardiac diseases.

ORGANISM(S): Homo sapiens

PROVIDER: GSE164490 | GEO | 2021/03/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Pericardial fluid microRNAs in patients with arrhythmogenic right ventricular cardiomyopathy or ischemic heart disease

Project description:Pericardial fluid microRNAs in patients with arrhythmogenic right ventricular cardiomyopathy or ischemic heart disease

| PRJNA690937 | ENA

The human pericardial fluid is enriched with cardiovascular-expressed microRNAs

Project description:The pericardial fluid (PF) surrounds the heart and it is contained in the pericardial sac. PF contains myocardial-derived factors. MicroRNAs (miRNAs) are negative post-transcriptional regulators of their target genes and they can be released into extracellular vesicles (EVs) contributing to cell-to-cell communication. We hypothesize that the PF contains miRNAs of myocardial origin and that represents a niche for the exchange of miRNAs between heart cells. In order to investigate whether PF contains functionally active miRNAs, miRNA expression profiles on PF samples collected from three patients undergoing aortic valve replacement (AVR) surgery performed during cardiopulmonary-bypass (CPB), were genereted.

2017-06-10 | GSE80577 | GEO

Characteristic molecular signature of pericardial effusion identifies malignant cancer in pericardial disorder patients

Project description:we examined 24 pericardial effusion patients and obtained pericardial fluid. To identify novel biomarker for detection cancer, detected transcriptome-based molecualr signature of compare pathologic cancer patients and non-cancer patients.

2019-12-31 | GSE118385 | GEO

Pericardial fluid exosome miRNA profiling

Project description:Pericardial sac surrounding the heart contains pericardial fluid (PF), which is rich in exosomes. PF exosomes increase angiogenesis in hypoxic endothelial cells and in animal model of hindlimb ischemia by passing the proangiogenic miRNAs to recipient cells. However, under pathological conditions such as diabetes, exosome cargo composition changes and harmful miRNAs can be transferred to the recipient cells and induce more deleterious effects in target tissues. In order to check cargo composition of different PF exosomes, we used PF exosomes from non-diabetic aortic valve replacement (AVR), mitral valve replacement (MVR), coronary artery bypass grafting (CABG) patients and CABG patients with diabetes.

2020-12-31 | GSE118103 | GEO

Pericardial fluid exosome miRNA profiling

Project description:Pericardial fluid exosome miRNA profiling

| PRJNA484411 | ENA

Characterization of pericardial fluid proteome through fractionation with magnetic nanoparticles (NPs@EDTA)

Project description:Despite the invasive nature of its collection, being in close contact to the heart, the pericardial fluid (PF) proteome reflects the pathophysiological status of this organ. Therefore, whenever it is available, e.g. on occasion of open-heart surgery, PF proteomic analysis can give important clues of the molecular mechanisms underlying heart disease and it may help uncover new diagnostic/prognostic markers as well as new therapeutic targets. Still, the characterization of its protein fraction is challenged by large amounts of albumin, that can be relatively higher than in plasma/serum. To help expand the PF catalogued to date and to validate the technique for future applications, we have fractionated and characterized the pericardial fluid, using N-(trimethoxysilylpropyl)ethylenediamine triacetic acid (EDTA)-functionalized magnetic nanoparticles (NPs@EDTA) followed by a GeLC-MS/MS approach. As compared to a traditional albumin and IgG-depletion kit, we found this method to be as efficient in removing albumin, with similar inter-individual proteome variability. Furthermore, the NPs@EDTA-based fractionation approach could expand the protein dynamic range and displayed good proteome reproducibility. Overall, 565 proteins were identified, with more than half being new assignments to PF proteome.

2018-01-09 | PXD008620 | Pride

Pathophysiology and therapeutics of arrhythmogenic right ventricular cardiomyopathy 5

Project description:Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) is an inherited cardiac disease characterized by fibro-fatty replacement of the myocardium that causes heart failure and sudden cardiac death. The most aggressive subtype of ARVC is ARVC type 5 (ARVC5), caused by a p.S358L mutation in TMEM43. The function and localization of TMEM43 and the mechanism by which the p.S358L mutation causes the disease, are unknown.

2019-07-12 | GSE101301 | GEO

Unique angiogenesis from cardiac arterioles during pericardial adhesion formation

Project description:The molecular mechanisms underlying postoperative pericardial adhesions are poorly understood. We aimed to unveil the temporal molecular and cellular mechanisms underlying tissue dynamics during adhesion formation, including inflammation, angiogenesis, and fibrosis. Using a previously established murine model, we successfully visualized the cell-based tissue dynamics during pericardial adhesion and discovered a unique angiogenic process for the induction of fibrosis. Masson’s trichrome staining revealed that collagen production was promoted from the fourth day after cardiac injury inflicted by talc injection into the pericardial cavity. A high degree of adhesion formation was observed during the stages in which collagen production was promoted. Histological analysis demonstrated that arterioles excessively sprouted from pericardial tissues in mice as well as in humans. The combination of RNA-seq and histological analyses revealed that hyperproliferative endothelial cells and myofibroblasts appeared in cytokine-exposed sprouting vessels and adhesion tissues, but not in quiescent vessels in the heart. Additionally, vascular smooth muscle cells were dedifferentiated from the contractile to the synthetic phenotype in heart tissue, and matrix metalloproteinase-dependent tissue remodeling in the pre-angiogenic stage potentially contributed to neovascularization and fibrosis in the pericardial cavity. Our findings will assist in developing prevention strategies for pericardial adhesions by targeting the recruitment of vascular cells from heart tissues.

2022-01-10 | GSE182735 | GEO

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

Project description:Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy primarily of the right ventricle characterized through fibrofatty replacement of cardiomyocytes. The genetic etiology in ARVC patients is most commonly caused by dominant inheritance and high genetic heterogeneity. Though histological examinations of ARVC affected human myocardium reveals fibrolipomatous replacement, the molecular mechanisms leading to loss of cardiomyocytes are largely unknown. We therefore analyzed the transcriptomes of 6 ARVC specimen derived from heart transplantation candidates and compared our findings to 6 non-failing donor hearts (NF) which could not be transplanted for technical reasons. In addition, we compared our findings to 7 hearts from patients with idiopathic dilated cardiomyopathy. From each heart left (LV) and right ventricular (RV) myocardial samples were analyzed by Affymetrix HG-U133 Plus 2.0 arrays, adding up to six sample groups. Unsupervised cluster analyses of the six sample groups revealed a clear separation of NF and cardiomyopathy samples. However, in contrast to the other samples, unsupervised cluster analyses revealed no distinct expression pattern in LV and RV samples from ARVC-hearts. We further identified differentially expressed transcripts using t-tests and found transcripts separating diseased and NF ventricular myocardium. Of note, in failing myocardium only about 15-16% of the genes are commonly regulated compared to NF samples. In addition both cardiomyopathies are clearly distinct on the transcriptome level. Comparison of the expression patterns between the failing RV and LV using a paired t-test revealed a lack of major differences between LV and RV gene expression in ARVC hearts. Microarrays were used to elucidate the differences between non-failing control hearts and those, suffering from arrhythmogenic right ventricular cardiomyopathy (ARVC).

2011-11-30 | E-GEOD-29819 | biostudies-arrayexpress

RNA-seq of zebrafish sa12692 mutants against WT controls

Project description:Arrhythmogenic Right Ventricular Cardiomyopathy is a congenital heart disorder characterized by fibrofatty replacement of the myocardium. The exact molecular mechanisms underlying the disease remain to be elucidated and treatment options are limited. The sa12692 mutant line contains a splice site mutation in the plakoglobin gene, resulting in the expression of a truncated protein. This protein is highly similar to the protein expressed in Naxos disease, a recessive form of ARVC. RNA-seq was used to investigate the effect of the sa12692 mutation on gene expression in order to uncover signalling pathways involved in the pathogenesis of ARVC. Gene expression was examined in whole larvae at 5 dpf and in hearts of 1 year old adult fish. Larvae at 5 dpf were selected as this timepoint is equivalent to birth in humans. Adult hearts were selected as ARVC is a disorder of the heart and cardiac symptoms generally manifest in adulthood. Hence, the molecular effect of the mutation could be profiled at two life stages.

2021-04-30 | E-MTAB-7920 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data