Genome-scale analysis of DNA methylation in rheumatic heart disease
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE84003 | GEO | 2016/07/06
SECONDARY ACCESSION(S): PRJNA327796
REPOSITORIES: GEO
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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). Genome-wide DNA methylation study is performed among 6 RHD-PAH patients and 6 healthy controls using Illumina HumanMethylation 450K array.
2016-07-06 | E-GEOD-84003 | biostudies-arrayexpress
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
Project description:Arterial pulmonary hypertension is a rare disease, with little knowledge regarding its etiology, and high mortality. Development of right and later on also left ventricular heart insufficiency, secondary to pulmonary hypertension, is a negative predictive factor. Genetic and molecular processes underlying left heart ventricle remodeling over the course of pulmonary hypertension remain unknown. In particular, there is no knowledge regarding the mechanisms of left heart ventricle atrophy which was completely avoided by researchers until recently.The aim of this study was to assess changes in protein abundance in left and right heart ventricle free wall of rats in monocrotaline model of PAH.
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Project description:Pulmonary arterial hypertension (PAH) is a common and serious complication of left-to-right shunt congenital heart disease (CHD).Some studies have provided evidence indicating that various circRNAs are abnormally expressed in pulmonary hypertension. However, the diagnostic value and biological functions of circRNAs in PAH remain largely elusive. To study the potential roles of circRNAs in PAH, we performed microarray analysis to identify circRNAs differentially expressed between pediatric patients with PAH due to CHD and control subjects.
2021-04-11 | GSE171827 | GEO
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.
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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.
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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.
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Project description:To investigate the underlying mechanism of pulmonary hypertension, the model of monocrotaline (MCT)-treated pulmonary arterial hypertension (PAH) rats were constructed to detect the differentially expressed profile of genes in lung tissue of PAH rat.
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Project description:Idiopathic pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by pulmonary arteriolar remodeling, and is frequently associated with right heart failure. This study identifies significant novel biological changes in eight genes and several genetic pathways, that were likely to contribute to the pathogenesis of PAH. We also demonstrate that PAH and PH secondary to idiopathic pulmonary fibrosis (IPF) are characterized by distinct gene expression signatures, implying distinct pathophysiological mechanisms. Keywords: disease versus control Keywords: Expression profiling by array
2010-01-22 | GSE15197 | GEO
Project description:Although multiple gene and protein expression have been extensively profiled in human pulmonary arterial hypertension (PAH), the mechanism for the development and progression of pulmonary hypertension remains elusive. Analysis of the global metabolomic heterogeneity within the pulmonary vascular system leads to a better understanding of disease progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung. The results suggest that PAH has specific metabolic pathways contributing to increased ATP synthesis for the vascular remodeling process in severe pulmonary hypertension. These identified metabolites may serve as potential biomarkers for the diagnosis of severe PAH. By profiling metabolomic alterations of the PAH lung, we reveal new pathogenic mechanisms of PAH in its later stage, which may differ from the earlier stage of PAH, opening an avenue of exploration for therapeutics that target metabolic pathway alterations in the progression of PAH. Global profiles were determined in human lung tissue and compared across 11 normal and 12 severe pulmonary arterial hypertension patients. Using a combination of microarray and high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung.
2014-11-14 | E-GEOD-53408 | biostudies-arrayexpress