Single cell RNA sequencing of human normal and failing heart
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE198784 | GEO | 2025/03/14
REPOSITORIES: GEO
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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:We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. We have established cistrome of four histone modifications and long-range chromatin interaction for enhancers and promoters in NF and DCM tissues. The differential histone modifications and E-P interactions were found in DCM, and these differences were associated with the gene expression level of a subset of disease-associated genes in human heart failure.
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Project description:We conducted chromatin immunoprecipitation followed by sequencing (ChIP-seq) and proximity ligation-assisted ChIP-seq (PLAC-seq) for enhancers and promoters (E-P) using left ventricular tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors. Differential active enhancer H3K27ac and promoter H3K4me3 regions were identified between NF and DCM. While the average read density (ARD) for H3K27ac is similar between NF and DCM, the ARD of H3K4me3 is significantly lower in DCM samples than in NF.Super-enhancer (SE) analysis revealed that 929 and 129 genes linked to NF- and DCM-specific SE, respectively, and three unique SE-associated genes between NF and DCM were identified.Moreover, the differential E-P interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. We have established cistrome of four histone modifications and long-range chromatin interaction for enhancers and promoters in NF and DCM tissues. The differential histone modifications and E-P interactions were found in DCM, and these differences were associated with the gene expression level of a subset of disease-associated genes in human heart failure.
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Project description:In ischemic cardiomyopathy (ICM), left ventricular systolic dysfunction leads to reduced blood flow and oxygen supply to the heart. Alterations in sarcomeric protein function and expression play prominent roles in the onset and progression of cardiomyopathies; however, the molecular mechanisms underlying ICM remain poorly defined. Herein, we have implemented a top-down liquid chromatography (LC)-mass spectrometry (MS)-based proteomics method for the simultaneous quantification of sarcomeric protein expression and modifications in non-failing donor (n = 16) compared to end-stage failing ICM (n = 16) human cardiac tissues. Our top-down proteomics platform provided a “bird’s eye view” of proteoform families with high mass accuracy and reproducibility. In addition, quantification of post-translational modifications (PTMs) and expression reveal significant changes in various sarcomeric proteins extracted from ICM tissues. Changes include altered phosphorylation and expression of cardiac troponin I (cTnI) and enigma homolog 2 (ENH2) as well as a marked increase in muscle LIM protein (MLP) and calsarcin-1 phosphorylation in ICM hearts. Our results imply that the contractile apparatus of the sarcomere is severely dysregulated during ICM. Thus, this study is the first to uncover significant molecular changes to multiple sarcomeric proteins in end-stage ischemic heart failure patients using LC-MS-based top-down proteomics.
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