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Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [snRNA-Seq]

ABSTRACT: Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [snRNA-Seq]

PROVIDER: PRJNA678355 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13057934.fastq.gz	Fastqsanger.gz
	SRR13057935.fastq.gz	Fastqsanger.gz
	SRR13057936.fastq.gz	Fastqsanger.gz
	SRR13057937.fastq.gz	Fastqsanger.gz
	SRR14513863.fastq.gz	Fastqsanger.gz

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Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [snRNA-Seq]

Project description:To generate the reference for cell composition deconvolution and characterize the cellular expression landscape, we performed single nucleus RNA-Seq (snRNA-Seq) on left ventricles from four non-failing hearts and one failing heart.

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Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction

Project description:Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction

| PRJNA678357 | ENA

Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [RNA-Seq]

Project description:Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [RNA-Seq]

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Chamber-enriched gene expression profiles in failing human hearts with reduced ejection fraction.

Project description:Heart failure with reduced ejection fraction (HFrEF) constitutes 50% of HF hospitalizations and is characterized by high rates of mortality. To explore the underlying mechanisms of HFrEF etiology and progression, we studied the molecular and cellular differences in four chambers of non-failing (NF, n = 10) and HFrEF (n = 12) human hearts. We identified 333 genes enriched within NF heart subregions and often associated with cardiovascular disease GWAS variants. Expression analysis of HFrEF tissues revealed extensive disease-associated transcriptional and signaling alterations in left atrium (LA) and left ventricle (LV). Common left heart HFrEF pathologies included mitochondrial dysfunction, cardiac hypertrophy and fibrosis. Oxidative stress and cardiac necrosis pathways were prominent within LV, whereas TGF-beta signaling was evident within LA. Cell type composition was estimated by deconvolution and revealed that HFrEF samples had smaller percentage of cardiomyocytes within the left heart, higher representation of fibroblasts within LA and perivascular cells within the left heart relative to NF samples. We identified essential modules associated with HFrEF pathology and linked transcriptome discoveries with human genetics findings. This study contributes to a growing body of knowledge describing chamber-specific transcriptomics and revealed genes and pathways that are associated with heart failure pathophysiology, which may aid in therapeutic target discovery.

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Gene expression in ischemic, end-stage failing and non-failing human hearts

Project description:A goal of this study was to identify and investigate previously unrecognized components of the remodeling process in the progression to heart failure by comparing gene expression in ischemic, failing (F) to non-failing (NF) hearts. These results also were compared to the changes observed in a proteomic analysis of F and NF hearts. RNA extracted from the left ventricle was hybridized to Affymetrix arrays to identify gene expression differences in ischemic, end-stage failing versus non-failing hearts. biological replicate: LV_NF_001, LV_NF002, LV_NF004, LV_NF005 biological replicate: LV_F_003, LV_F005, LV_F009, LV_F006

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Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction

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