Microbiome and Metabolome in Ischaemic Heart Disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB46098 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9538790.fastq.gz | Fastqsanger.gz | |||
| ERR9538800.fastq.gz | Fastqsanger.gz | |||
| ERR9538810.fastq.gz | Fastqsanger.gz | |||
| ERR9538820.fastq.gz | Fastqsanger.gz | |||
| ERR9538830.fastq.gz | Fastqsanger.gz |
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Project description:Coronary artery disease (CAD) and ischaemic cardiomyopathy are leading causes of mortality and morbidity worldwide. Currently there are only two well established biomarkers used for heart failure diagnosis and prognosis. Therefore, more research into the genetic and epigenetic mechanisms of heart failure (HF) will allow identification of biomarkers that can be used for different stages of HF. DNA methylation is an epigenetic mark that is increasingly recognised to play a critical role in cardiovascular disease. However, there are no methylation studies that specifically focus on ischaemic cardiomyopathy. Here we performed a small scale methylome wide association study to identify epigenetic markers in peripheral blood in a cohort of patients with and without HF who otherwise share a similar coronary ischaemic burden, age, sex, and ethnicity. We identified 68 significantly differentially methylated regions in our data. Of these regions, 48 occurred within gene bodies and 25 were located near enhancer elements, some within coding genes and some in non-coding genes. Our gene set enrichment analyses identified 103 significantly enriched gene sets in HF. We have demonstrated the utility of methyl-binding domain capture sequencing to evaluate DNA methylation markers in a perioperative cohort of cardiac surgical patients with ischaemic cardiomyopathy and HF. The peripheral methylation status of specific coding genes, such as HDAC9, are candidates for larger longitudinal studies. We have further demonstrated the value and feasibility of examining DNA methylation patterns from peripheral blood to highlight cellular pathways and processes that may contribute to the development of HF.
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Project description:Background: Lamins A/C (encoded by the LMNA gene) can lead to dilated cardiomyopathy (DCM). Objectives: This study sought to undertake proteomic analysis of myocardial tissue to explore the postgenomic phenotype of end-stage lamin heart disease. Methods: Consecutive patients with end-stage lamin heart disease (LMNA-group, n=7) and ischaemic DCM (ICM-group, n=7) undergoing heart transplantation were enrolled. Samples were obtained from left atrium(LA), left ventricle(LV), right atrium(RA), right ventricle(RV) and interventricular septum(IVS). Liquid chromatography combined with mass-spectrometry was used for protein quantification. We compared protein concentrations in cardiac samples between LMNA and ICM groups. Proteins were considered differentially abundant if the quantitative difference was 1.5-fold and corrected p-value <0.05 at a false discovery rate of 0.01. Gene ontology(GO) enrichment analysis explored the related biological processes. Results: 4,247 proteins were identified in LMNA and ICM samples, of which 633 were differentially abundant in LA, 39 in LV, 181 in RA, 52 in RV, and 85 in IVS. Abundance of lamin A/C was reduced but lamin B (LMNB) increased in LMNA LA/RA tissue compared to ICM, but not in LV/RV. Transthyretin was more abundant in the LV/RV of LMNA compared to ICM while sarcomeric proteins such as titin and cardiac myosin heavy chain were generally reduced in RA/LA of LMNA. Protein expression profiling and GO enrichment analysis revealed sarcopenia, extracellular matrix(ECM) remodeling, deficient myocardial energetics, redox imbalances, and abnormal calcium handling in LMNA samples. Conclusion: Lamin heart disease is a biventricular and biatrial disease, characterized by sarcopenia, aberrant metabolism, and ECM remodeling. LMNB and transthyretin were unexpectedly abundant in the atria and ventricles respectively of patients with end-stage lamin heart disease potentially hinting to the possibility of compensatory responses.
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