ABSTRACT: Methylome analysis reveals alterations in DNA methylation in the regulatory regions of left ventricle development genes in human dilated cardiomyopathy (methylation)
Project description:Methylome analysis reveals alterations in DNA methylation in the regulatory regions of left ventricle development genes in human dilated cardiomyopathy
Project description:Methylome analysis reveals alterations in DNA methylation in the regulatory regions of left ventricle development genes in human dilated cardiomyopathy (mRNA)
Project description:A comparison of epigenetic nuclear DNA methylation and gene expression changes between human dialated cardiomypathy left ventricle samples and non-failing cardiac left ventricule samples This study addresses how depletion of huaman cardiac left ventricle mitochondrial DNA and epigentic nuclear DNA methylation promote cardiac dysfunction in human dilated cardiomyopathy.
Project description:A comparison of epigenetic nuclear DNA methylation and gene expression changes between human dialated cardiomypathy left ventricle samples and non-failing cardiac left ventricule samples This study addresses how depletion of huaman cardiac left ventricle mitochondrial DNA and epigentic nuclear DNA methylation promote cardiac dysfunction in human dilated cardiomyopathy. Each sample was fluorescently labeled and hybridized to Roche Nimblegen 2.1M Deluxe Promoter Arrays and Expression arrays.
Project description:Alterations in DNA methylation and gene expression have been implicated in the development of human dilated cardiomyopathy (DCM). In this study, we analyzed DNA methylomes (Infinium 450K HumanMethylation BeadChip) and characterize differentially methylated probes between the left and right ventricles Illumina 450K array and HT-12 v4 array for the left, right ventricles
Project description:Alterations in DNA methylation and gene expression have been implicated in the development of human dilated cardiomyopathy (DCM). In this study, we analyzed DNA methylomes (Infinium 450K HumanMethylation BeadChip) and characterize differentially methylated probes between the left and right ventricles
Project description:Alterations in DNA methylation and gene expression have been implicated in the development of human dilated cardiomyopathy (DCM). In this study, we analyzed DNA methylomes (Infinium 450K HumanMethylation BeadChip) and transcriptomes (Infinium HT-12 v4) to characterize differentially methylated probes (DMPs) and differentially expressed genes (DEGs) between the left and right ventricles of human DCM. Illumina 450K array and HT-12 v4 array for the left, right ventricles
Project description:Alterations in DNA methylation and gene expression have been implicated in the development of human dilated cardiomyopathy (DCM). In this study, we analyzed DNA methylomes (Infinium 450K HumanMethylation BeadChip) and transcriptomes (Infinium HT-12 v4) to characterize differentially methylated probes (DMPs) and differentially expressed genes (DEGs) between the left and right ventricles of human DCM.
Project description:The left and right ventricles of the human heart are functionally and developmentally distinct such that genetic or acquired insults can cause dysfunction in one or both ventricles resulting in heart failure. First, we performed unbiased quantitative mass spectrometry on the myocardium of 25-27 pre-mortem cryopreserved non-diseased human hearts to compare the metabolome and proteome between the normal left and right ventricles. Constituents of gluconeogenesis, glycolysis, lipogenesis, lipolysis, fatty acid catabolism, the citrate cycle and oxidative phosphorylation were down-regulated in the left ventricle, while glycogenesis, pyruvate and ketone metabolism were up-regulated. Inter-ventricular significance of these metabolic pathways was then found to be diminished within end-stage dilated cardiomyopathy and ischaemic cardiomyopathy (n = 30-33), while heart failure-associated pathways were increased in the left ventricle relative to the right within ischaemic cardiomyopathy, such as fluid sheer-stress, increased glutamine to glutamate ratio, and down-regulation of contractile proteins indicating a left ventricular pathological bias.
