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Unravelling the etiology of dilated cardiomyopathy through differential miRNA-mRNA interactome

ABSTRACT: Unravelling the etiology of dilated cardiomyopathy through differential miRNA-mRNA interactome

PROVIDER: PRJNA1018441 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26088052.fastq.gz	Fastqsanger.gz
	SRR26088053.fastq.gz	Fastqsanger.gz
	SRR26088054.fastq.gz	Fastqsanger.gz
	SRR26088055.fastq.gz	Fastqsanger.gz
	SRR26088056.fastq.gz	Fastqsanger.gz

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Unravelling the etiology of dilated cardiomyopathy through differential miRNA-mRNA interactome

Project description:Dilated cardiomyopathy (DCM) entails a broad group of diseases, acquired or genetic, that share a similar phenotype. The understanding of gene-specific pathogenetic mechanisms and the determination of the functional effects of each variant may tailor different therapeutic strategies. MicroRNAs (miRNAs) are short sequences of non-coding RNA that play an important role in the development of several cardiovascular diseases, including DCM. Here, we applied mRNA and small RNA sequencing to identify the gene and miRNA signature from myocardial biopsies from four patients with DCM caused by volume overload (VCM) and four with ischemic DCM (ICM). Analysis showed five miRNAs and 112 mRNAs dysregulated in VCM vs ICM. Differentially expressed genes were positively enriched for extracellular matrix (ECM), mitochondria respiration-related, cardiac muscle contraction and fatty acid pathways in VCM vs ICM, and negatively enriched for immune response-related pathways, JAK-STAT and NF-kappa B signaling pathways in VCM vs ICM. miRNA-mRNA interaction analysis revealed four negatively correlated miRNA-target transcript pairs, miR-218-5p-DDX6, miR-218-5p-TT39C, miR-218-5p-SEMA4A and miR-494-3p-SGMS2. qRT-PCR validation showed a strong correlation between RNA-seq and qRT-PCR for these genes and miRNAs. These findings suggest that transcriptome signatures may distinguish distinct etiologies of DCM shedding light on underlying biological differences between VCM and ICM.

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Project description:Unravelling Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy [miRNA-seq]

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Unravelling Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy [mRNA-seq]

Project description:Unravelling Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy [mRNA-seq]

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Unravelling Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy [mRNA-seq]

Project description:Arrhythmogenic cardiomyopathy is an inherited entity characterized by irregular cell-cell adhesion, cardiomyocyte death, fibro-fatty replacement of ventricular myocytes, leading to malignant ventricular arrythmias, contractile dysfunction and sudden cardiac death. Pathogenic variants in genes that encode desmosome are the predominant cause of arrhythmogenic cardiomyopathy. Moreover, signalling pathways such as Wnt/ß-catenin and transforming growth factor-β have been involved in the disease progression. However, still little is known about the molecular pathophysiological mechanisms that underlie arrhythmogenic cardiomyopathy pathogenesis. We used mRNA and small RNA sequencing to analyse the transcriptome of health and arrhythmogenic cardiomyopathy autopsied human hearts. Our results showed 697 differentially expressed genes, and eight differentially expressed miRNAs. Functional enrichment revealed mitochondrial respiratory-related pathways, impaired response to oxidative stress, apoptotic signalling pathway, inflammatory response-related and extracellular matrix response pathways. Furthermore, analysis of miRNA-mRNA interactome identified eleven negatively correlated miRNA-target pairs for arrhythmogenic cardiomyopathy. Our finding revealed novel arrhythmogenic cardiomyopathy-related miRNAs with important regulatory function in disease pathogenesis highlighting their value as potential key targets for therapeutic approaches.

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Project description:This study attempts at investigating the changes in cardiac gene expression that occur in Dilated Cardiomyopathy (DCM). DCM in Dobermans and Boxers are the focus of this study. Control heart tissue as well as Pacing tissue used is from mongrel dogs. Keywords: control vs pacing vs disease; strain specific disease 3 Dobermans-DCM, 4 Boxers-DCM, 3 mongrels-control and 3 mongrels-pacing

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Dilated Cardiomyopathy and Non Failing Biopsies

Project description:Dilated cardiomyopathy (DCM) is a common cause of heart failure and a leading cause of cardiac transplantation in western countries. The robust predictive expression profile of cardiomyopathic and NF hearts as well as the functional classification can help to identify promising candidates for DCM and may improve the early diagnosis of cardiomyopathy. Keywords: disease state analysis

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Project description:Cardiac metabolism is deranged in heart failure, but underlying mechanisms remain unclear. Lysine demethylase 8 (Kdm8) represses gene expression in the embryo and controls metabolism in cancer. However, its function in cardiac homeostasis is unknown. We show that Kdm8 maintains a mitochondrial gene network active by repressing Tbx15 to prevent dilated cardiomyopathy leading to lethal heart failure. Deletion of Kdm8 in mouse cardiomyocytes increased H3K36me2 with activation of Tbx15 and repression of target genes in the NAD+ pathway before dilated cardiomyopathy initiates. Moreover, NAD+ supplementation prevented dilated cardiomyopathy in Kdm8 mutant mice and TBX15 overexpression blunted NAD+-activated cardiomyocyte respiration. Furthermore, KDM8 was downregulated in human hearts affected by dilated cardiomyopathy and higher TBX15 expression defines a subgroup of affected hearts with the strongest downregulation of genes encoding mitochondrial proteins. Thus, KDM8 represses TBX15 to maintain cardiac metabolism. Our results suggest that epigenetic dysregulation of metabolic gene networks initiates myocardium deterioration towards heart failure and could underlie heterogeneity of dilated cardiomyopathy.

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