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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1

ABSTRACT: LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1

PROVIDER: PRJNA1019725 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26141116_1.fastq.gz	Fastqsanger.gz
	SRR26141116_2.fastq.gz	Fastqsanger.gz
	SRR26141117_1.fastq.gz	Fastqsanger.gz
	SRR26141117_2.fastq.gz	Fastqsanger.gz
	SRR26141118_1.fastq.gz	Fastqsanger.gz

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

Project description:LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (Iso-seq)

Project description:Dilated cardiomyopathy (DCM) is characterized by left ventricular dilation and continuous systolic dysfunction. Mitochondrial impairment is critical in DCM, but the mechanism remains to be elucidated. Here we explored the cardio-protective role of a heart-enriched long non-coding RNA (lncRNA), named dilated cardiomyopathy repressive transcript (DCRT), via maintaining mitochondrial function. We found the lncRNA DCRT was highly enriched in normal heart tissue and its expression was significantly down-regulated in myocardium of DCM patients. DCRT knockout in mice spontaneously developed cardiac dysfunction with cardiac enlargement and mitochondrial impairment. DCRT transgenic or overexpressed mice attenuated cardiac dysfunction induced by transverse aortic constriction (TAC) treatment.

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:We aimed to identify aberrantly expressed lncRNA and mRNA expression profiles of dilated cardiomyopathy (DCM) and explore their potential functions. 8 DCM blood samples and paired healthy control blood samples underwent RNA-sequence.

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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

2008-05-08 | E-GEOD-11015 | biostudies-arrayexpress

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 [RNA-seq]

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.

2022-12-23 | GSE215351 | GEO

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