Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

43 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-scale analysis of DNA methylation in rheumatic heart disease

ABSTRACT: The aim of the current study is to identify DNA methylation markers associated with rheumatic heart disease with secondary pulmonary arterial hypertension (RHD-PAH). Genome-wide DNA methylation study is performed among 6 RHD-PAH patients and 6 healthy controls using Illumina HumanMethylation 450K array.

ORGANISM(S): Homo sapiens

SUBMITTER: Shiwei Duan

PROVIDER: E-GEOD-84003 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-scale analysis of DNA methylation in rheumatic heart disease

Project description:The aim of the current study is to identify DNA methylation markers associated with rheumatic heart disease with secondary pulmonary arterial hypertension (RHD-PAH).

2016-07-06 | GSE84003 | GEO

Profiling system-wide variations between Acute Rheumatic Fever and Rheumatic Heart Disease

Project description:Rheumatic heart disease (RHD) continues to affect developing countries with low income, due to the lack of resources and effective diagnostic techniques. Understanding the genetic basis of progression from its prequel disease state, acute rheumatic fever (ARF), would aid in developing predictive biomarkers and improving patient care. To gain system-wide molecular insights into possible causes for progression, we collected blood transcriptomes from ARF (5) and RHD (5) patients. Using an integrated transcriptome and network analysis, we identified a subnetwork comprising the most significantly differentially expressed genes and most perturbed pathways in RHD as compared to ARF. For example, the chemokine signaling pathway was seen to be upregulated while tryptophan metabolism was found to be downregulated in RHD. The subnetworks of variation between the two conditions provide unbiased molecular-level insights into the host processes that may be associated with the progression of ARF to RHD, which has the potential to inform future diagnostics and therapeutic strategies. We also found significantly raised neutrophil/lymphocyte ratio in both ARF and RHD cohorts. Activated neutrophils and inhibited NK cell gene signatures reflected the drivers of the inflammatory process being common to both the disease conditions.

2022-07-29 | GSE209591 | GEO

Endothelial DNA methalytion signature in pulmonary arterial hypertension

Project description:Pulmonary arterial hypertension (PAH) is a severe and incurable pulmonary vascular disease. One of the primary origins of PAH is pulmonary endothelial dysfunction leading to vasoconstriction, aberrant angiogenesis and smooth muscle cell proliferation, endothelial-to-mesenchymal transition, thrombosis and inflammation. Our objective was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation. DNA was extracted from cultured PEC from patients with idiopathic PAH (n=11), heritable PAH (n=10) and controls (n=18). ). DNA methylation was assessed using the Illumina HumanMethylation450 Assay. After normalization, samples and probes were clustered according to their methylation profile. Differential clusters were functionally analysed using bioinformatics tools.

2016-07-15 | E-GEOD-84395 | biostudies-arrayexpress

Genomic analysis of lncRNA and mRNA profile in circulating exosomes of patients with rheumatic heart disease

Project description:Rheumatic heart disease (RHD) is still a serious life-threatening heart disease in developing countries. Accumulating evidence suggested that circulating exosomes and its cargoes including mRNA, microRNA and long noncoding RNA (lncRNA) play essential roles in cardiovascular diseases, while their roles in RHD remain unexplored. In the present study, we investigated genomic profiles of circulating exosomes harvested from RHD patients. And we performed gene ontology (GO) and pathway analysis to explore potential roles of differentially expressed mRNAs. Furthermore, we identified 5 lncRNAs and their flanking coding genes simultaneously dysregulated in the circulating exosome. Collectively, we provided the first transcriptome analysis identifying lncRNAs and mRNAs in circulating exosomes in RHD patients, and our data provide valuable insights into seeking for potential biomarkers and therapeutic targets for RHD.

2019-04-19 | GSE130033 | GEO

Altered expression of transfer-RNA-derived small RNAs (tsRNAs) in human with rheumatic heart disease

Project description:Rheumatic heart disease (RHD) remains a serious public health problem in developing countries. Atrial fibrillation (AF) is a medical complication of RHD. Although the understanding of disease pathogenesis has advanced in recent years, the key questions need to be addressed. Transfer RNA–derived small RNAs (tsRNAs) are a novel type of short non-coding RNAs that have potential regulatory functions in various physiological and pathological processes. The present study used tsRNAs sequencing to investigate the relationship between RHD and atrial fibrillation (AF). Three paired myocardial papilla were taken from six rheumatic RHD patients with AF (3 cases) or without AF (3 cases) from January 2016 to January 2017 in Xiangya Hospital, Central South University. A total of 219 precisely matched tsRNAs were identified, and 77 tsRNAs (fold change > 2.0 and P < 0.05) were differently changed. Three tsRNAs (AS-tDR-001269, AS-tDR-001363, AS-tDR-006049) were randomly selected and verified by qRT-PCR. The results of qRT-PCR were consistent with tsRNAs sequencing, suggesting the tsRNAs sequencing was reliable. Then bioinformatics analysis indicated that the target genes were abundant in regulation of transcription, DNA binding, intracellular. Most of the genes were predicted to interplay with cytokine-cytokine receptor by KEGG analysis. Our findings uncover the pathological process of AF in RHD through tsRNAs sequencing. This study provides new ideas for future research on elucidating the mechanism of AF in RHD and offers potential new candidates for the treatment and diagnosis of RHD.

2021-12-23 | GSE185581 | GEO

Endothelial DNA methalytion signature in pulmonary arterial hypertension

2016-07-15 | GSE84395 | GEO

The expression of microRNA-30 family in pulmonary arterial hypertension

Project description:miRNAs have been proved to participate in the regulation of proliferation and apoptosis in many diseases,we consider there may be associations between miRNAs and development of pulmonary arterial hypertension (PAH). Previous studies have revealed that several miRNAs participated in the regulation of the development of PAH. In this study, we investigated the miRNA differential expression spectrum in pulmonary arterial hypertension patients.

2021-10-01 | E-MTAB-10932 | biostudies-arrayexpress

Acquired chromosome abnormalities in the lungs of patients with Pulmonary Arterial Hypertension (Illumina)

Project description:Vascular remodeling in pulmonary arterial hypertension (PAH) involves proliferation and migration of endothelial and smooth muscle cells, leading to obliterative vascular lesions. Previous studies have indicated that the endothelial cell proliferation is quasi-neoplastic, with evidence of monoclonality and instability of short DNA microsatellite sequences. To assess whether there is larger scale genomic instability, we performed genome-wide microarray copy number analysis on pulmonary artery endothelial (PAEC) and smooth muscle cells isolated from the lungs of PAH patients. Mosaic chromosomal abnormalities were detected in five of nine PAEC cultures from PAH lungs and zero of four controls. Fluorescent in situ hybridization analysis confirmed the presence of these abnormalities in vivo in two of three cases. One patient harbored a germline mutation of BMPR2, the primary genetic cause of PAH, and a somatic loss of chromosome-13, which constitutes a second hit in the same pathway by deleting Smad-8. In two female cases with mosaic loss of the X-chromosome, methylation analysis showed that the active X was deleted. Remarkably, one also showed completely skewed X-inactivation in the non-deleted cells, suggesting the PAEC population was clonal prior to the acquisition of the chromosome abnormality. Our data indicate a high frequency of genetically abnormal sub-clones within the lung vessels of patients with PAH and provide the first definitive evidence of a second genetic hit in a patient with a germline BMPR2 mutation. We propose that these chromosome abnormalities may confer a growth advantage and thus contribute to the progression of PAH. Cross-sectional study of genomic copy number in cells cultured from the lungs of PAH patients.

2010-05-01 | E-GEOD-21097 | biostudies-arrayexpress

Expression data analysis in lungs from mice induced for pulmonary arterial hypertension (PAH) by inhalation of Stachybotrys chartarum spores

Project description:It has been reported that repeated intra-tracheal instillation of S. chartarum spores induced significant pulmonary arterial remodeling in mice, which resulted in pathological changes like human pulmonary arterial hypertension (PAH) and elevation right ventricle systolic pressure. Then, we used microarrays to know the complex molecular mechanisms that underlie pathogenesis of PAH.

2010-07-29 | GSE23178 | GEO

Effects of ACE2 on BMPR2 mutation-mediated defects in gene expression

Project description:BMPR2 mutation causes pulmonary arterial hypertension (PAH); ACE2 treatment can resolve established BMPR2-mediated PAH. The purpose of this study was to uncover the molecular mechanism behind this.

2010-08-25 | GSE21583 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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