Expression profiles of tRNA-derived small RNAs in epicardial adipose tissue of patients with heart failure
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE210707 | GEO | 2022/08/11
REPOSITORIES: GEO
Similar Datasets
Project description:Atrial fibrillation (AF) is the most common sustained arrythmia, but the potential molecular indicators involved in structural and electronical remodeling remains to be clarified. Epicardial adipose tissue (EAT), a visceral fat depot surrounding the heart, is increasingly recognized to be metabolically active and has been proposed with an arrthymogenicity nature. It is able to secret a myriad of bioactive molecules, including exosomes carrying tRNA derived small RNAs (tsRNAs). Accumulating findings have suggested that these specific tsRNAs dynamically impact fundamental cellular processes, but there are no studies discovering the association between tsRNAs of EAT and AF, and their interactions and potential signaling pathways remain to be elucidated.
2022-08-11 | GSE210705 | GEO
Project description:Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot closely linked to the pathogenesis of heart failure (HF). But the molecular signatures related to the mechanism of HF have not been systematically explored. Here, we present comprehensive proteomic analysis of EAT in HF patients and non-HF subjects as controls. A total of 771 proteins were identified in liquid chromatography-tandem mass spectrometry experiments. Among them, 17 increased in abundance in HF and 7 decreased. They were involved in HF-related processes including inflammation and oxidative stress response and lipid metabolism. Of these proteins, Serine proteinase inhibitor A3 (Serpina3) levels in EAT were highly upregulated in HF, with HF/non-HF ratio of 4.63 and a P value of 0.0047. Gene expression of Serpina3 via quantitative polymerase chain reaction was significantly increased in the HF group. ELISA analysis confirmed a significant increase in circulating plasma Serpina3 levels in the HF group (P = 0.004). In summary, for the first time we describe EAT proteome as a possible trigger for HF. Our profiling provides a comprehensive basis for linking EAT with pathogenesis of HF. Understanding the role of EAT may offer new insights into the treatment of HF.
2020-05-26 | PXD014592 | Pride
Project description:Background: Heart failure with preserved ejection fraction (HFpEF) has become a major public health problem with a morbidity and mortality similar to heart failure with reduced ejection fraction (HFrEF). Recently, it has been proved epicardial adipose tissue (EAT) played an important role in the pathogenesis of HFpEF, however the underlying mechanisms are not yet fully elucidated. This study attempted to describe comprehensive proteomic analysis of EAT in HFpEF patients and non-HF patients as controls, and identify local candidate molecules characterizing EAT in HFpEF patients. EAT samples were collected from patients undergoing heart surgery in two groups. Proteins was identified in liquid chromatography-tandem mass spectrometry (LC-MS/MS) experiments. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was conducted and protein-protein interaction network was constructed with Cytoscape software. A total of 2416 proteins were identified in LC-MS/MS experiments and 2349 proteins were quantified. Amongst them, totally 96 significant proteins (including 71 upregulated proteins in abundance and 25 downregulated proteins) were differently expressed between HFpEF and non-HF group. GO-enrichment, KEGG pathway analysis and interaction network construction showed these differentially expressed proteins were predominantly involved in HFpEF-related processes including lipid metabolic disorder, inflammation and mitochondrial dysfunction including FABP5, CD36, CFB, ADSL, POSTN, TRAP1 et al., which might contribute to the pathogenesis of HFpEF. In conclusion, this is the first demonstration to describe the parts of EAT proteome in HFpEF patients. Our findings provide a comprehensive understanding for linking EAT to the pathogenesis of HFpEF, which may offer new insights into the treatment of HFpEF targeting on EAT.
2023-01-30 | PXD028158 | Pride
Project description:Recent studies have suggested that epicardial adipose tissue (EAT) play an important role in the pathogenesis of heart failure with preserved ejection fraction (HFpEF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that molecules secreted from EAT, including exosomes carrying non-coding RNAs (ncRNAs), may participate in the development of HFpEF. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with HFpEF.
2022-01-05 | GSE192886 | GEO
Project description:The biological functions of epicardial adipose tissue (EAT) remain largely elusive. However, the proximity of EAT to the coronary arteries suggests a role in the pathogenesis of coronary artery disease (CAD). Objectives of this study were to identify genes that are up- or down-regulated among three adipose tissues (AT), namely EAT, mediastinal (MAT) and subcutaneous (SAT) and to study their possible relationships with the development of cardiovascular diseases. Samples were collected from patients undergoing coronary artery bypass grafting surgeries. Gene expression was evaluated in all three AT depots of six men using the lllumina® HumanWG-6 v3.0 expression BeadChips. Twenty-two and 73 genes were up-regulated in EAT compared to mediastinal and subcutaneous AT, respectively. Ninety-four genes were down-regulated in EAT compared to subcutaneous adipose depot. However, none were significantly down-regulated in EAT compared to mediastinal fat. More specifically, the expression of the adenosine A1 receptor (ADORA1), involved in myocardial ischemia, was significantly up-regulated in EAT. Levels of the prostaglandin D2 synthase (PTGDS) gene, recently associated with the progression of atherosclerosis, were significantly different in the three pairwise comparisons (epicardial > mediastinal > subcutaneous). The results of ADORA1 and PTGDS were confirmed by qPCR in 25 biological replicates. Overall, the transcriptional profiles of EAT and MAT were similar compared to the subcutaneous compartment. Despite this similarity, two genes involved in cardiovascular diseases, ADORA1 and PTGDS, were up-regulated in EAT. These results provide insights about the biology of EAT and its potential implication in CAD. Samples of epicardial, mediastinal and subscutaneous adipose tissue were collected from the chest of 6 male patients undergoing coronary artery bypass grafting surgeries. The RNA was labeled and hybridized using a standard Illumina protocol (https://icom.illumina.com/Login?ReturnUrl=%2ficom%2fsoftware.ilmn%3fid%3d214&id=214). Three pairwise comparison among the three adipose tissue were made using significance analysis of microarrays.
2011-05-17 | E-GEOD-24425 | biostudies-arrayexpress
Project description:The main goal of this study was to examine the presence and specific transcriptomic profile of epicardial adipose tissue (eAT) in zebrafish. We assessed how cold treatment affects the epicardial adipose tissue. Additional we provided some key differences between human, mouse and zebrafish epicardial adipose tissue.
2024-03-19 | GSE227670 | GEO
Project description:Epicardial adipose tissue (EAT) inflammation is thought to potentiate the development of coronary artery disease (CAD). Overall diet quality and statin therapy are important modulators of inflammation and CAD progression. Our objective was to examine the effects and interaction of dietary patterns and statin therapy on EAT gene expression in the Ossabaw pig.
2020-02-04 | GSE129301 | GEO
Project description:The primary objective of the study was to investigate the uncoupling protein-1 (UCP1) associated features of human epicardial adipose tissue (eAT) using next generation deep sequencing. In addition, paired mediastinal adipose tissue (mAT) and subcutaneous adipose tissue (sAT) samples colleced from patients undergoing cardic surgeries at our center were included in the study.
2019-06-10 | GSE125856 | GEO
Project description:Accumulating studies have suggested that epicardial adipose tissue play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying non-coding RNAs, may modulate atrial remodeling. The aim of the present study was to investigate the expression profile of mRNAs and ncRNAs in EAT with AF.
2019-08-07 | GSE135445 | GEO
Project description:The epicardial adipose tissue (EAT) is a visceral adipose tissue in close contact with coronary vessels whose increase is associated with coronary artery disease (CAD). Our goal was to identify candidate molecule(s) characterizing EAT which could intervene in the pathogenesis of CAD. An approach combining microarrays and bioinformatic sequence analysis tools for predicting secreted proteins (TargetP) was applied to paired biopsies of subcutaneous adipose tissue (SAT) and EAT, obtained from patients with or without CAD (NCAD). Results were validated in 3 independent groups of subjects by RT-qPCR, western blot, immuno histochemistry and explants secretion. sPLA2-IIA ranked first among genes coding for potentially secreted proteins with the highest overexpression in EAT in both CAD and NCAD. RT-qPCR confirmed its increased expression in EAT ( p<0.01) and in EAT from CAD as compared to NCAD (49.3 ±13 vs. 17.4 ± 9.7 p<0.01). sPLA2-IIA protein level was higher in EAT than in SAT. EAT explants demonstrated also significantly higher sPLA2-IIA secretion levels than SAT ones (4.37±2.7 vs 0.67± 0.28 ng.ml-1/g tissue/24h,p<0.03). sPLA2-IIA labeling was evidenced in EAT in the stroma vascular fraction between adipocytes and in connective capsules, with no immunostaining of the adipocytes. SAT was weakly labeled following the same pattern. Conclusion: We evidenced for the first time an increased expression of sPLA2-IIA in EAT from patients with CAD, a phospholipase that was shown to be an independent risk factor for CAD. These findings suggest a potentially pathophysiological role of EAT in CAD.
2021-10-20 | GSE18612 | GEO