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Characterization of extrachromosomal circular DNA for human dilated cardiomyopathy

ABSTRACT: Characterization of extrachromosomal circular DNA for human dilated cardiomyopathy

PROVIDER: PRJNA1008715 | ENA |

REPOSITORIES: ENA

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Characterization of extrachromosomal circular DNA for human dilated cardiomyopathy

Project description:Extrachromosomal circular DNAs (eccDNAs) are prevalent in different tumors, and have been shown to be important oncogenic drivers. While recent studies have found many eccDNAs in non-tumor cells, to date, the nature and characteristics of eccDNAs in human heart failure are rarely known. In this study, we provided a comprehensive analysis of eccDNAs in human heart failure caused by dilated cardiomyopathy (DCM). Using the Circle-Seq method, we identified the expression profile of eccDNAs in heart samples from DCM patients and healthy controls. Most eccDNAs were less than 1kb and enriched in two peaks. Analysis of the genomic distribution of eccDNAs revealed that eccDNAs were derived from all chromosomes and half of these eccDNAs carried at least one gene or gene fragment. Most eccDNAs originated from 5’UTR, 3’UTR, CpG island, long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs). In addition, eccDNAs were more enriched on gene-rich chromosomes 17 and 19. In conclusion, our work delineated the eccDNAs profiling of human healthy heart and DCM and explored potential functions of eccDNAs in the development of DCM.

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Differential expression profiles and functional prediction of circular RNAs in pediatric dilated cardiomyopathy

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Analysis of changes in circular RNA expression in human dilated cardiomyopathy

Project description:Circular RNAs (circRNAs) have been reported to play important roles in various cardiovascular diseases. However, their expression profile in human dilated cardiomyopathy (DCM) has not been fully elucidated. In our study, heart samples from DCM patients and healthy controls were used to identify circRNAs by high-throughput sequencing. A total of 9585 circRNAs were identified in the DCM and control groups. To assess the differentially expressed circRNAs, the criteria were set as a fold change of ≥ 2 or ≤ 0.5 and a P value of < 0.05. Compared with circRNAs in the control group, 298 dysregulated circRNAs were identified in patients with DCM, of which 231 were upregulated and 85 were downregulated. In conclusion, our study evaluated cardiac circRNA expression in DCM by high-throughput sequencing and provide a foundation for future studies of circRNAs in DCM.

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Dilated Cardiomyopathy in Dobermans and Boxers

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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Differential expression profiles and functional prediction of circular RNAs in pediatric dilated cardiomyopathy

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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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KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy [CUT&Tag]

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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