Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The atlas of the human hypertrophied heart reveals impaired cell communication

ABSTRACT: Pathological cardiac hypertrophy is a leading cause of heart failure. The understanding of disease mechanisms is primarily based on experimental models, but knowledge of the full repertoire of cardiac cells and their gene expression profiles in the human heart is missing. Here, using large-scale single-nucleus transcriptomes, we highlight the transcriptional response of cardiomyocytes to pressure overload in humans with stenosis of the aortic valve and disclose major alterations in cellular cross-talk. Cardiomyocytes showed a reduction of incoming connections with endothelial cells and fibroblasts. Particularly Eph receptor tyrosine kinases, including the predominant EPHB1 gene, were significantly down-regulated in cardiomyocytes of the hypertrophied heart. We compared 5 AS patients to healthy patients from the human heart cell ATLAS (https://www.heartcellatlas.org). This repository contains the processed files from the single nuclei RNA-SEQ.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: David John

PROVIDER: E-MTAB-11268 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Single nuclei sequencing of human and Mice HFrEF data (Heart Failure with reduced ejection fraction)

Project description:Here we provide snRNA-seq datasets from heart failure patients with reduced ejection fraction and snRNA-SEQ of the corresponding LAD mouse model (permanent ligation of the left anterior descending artery)

2023-08-20 | E-MTAB-13264 | biostudies-arrayexpress

Single Nuclei Sequencing of old and young mice hearts under senolytica (Ageing impairs the neuro-vascular interface in the heart)

Project description:Aging is a major risk factor for impaired cardiovascular health. The aging myocardium is characterized by microcirculatory and diastolic dysfunction and increased susceptibility to arrhythmias. Nerves align with vessels during development. However, the impact of aging on the cardiac neuro-vascular interface is entirely unknown. Here, we report that aging reduces nerve density specifically in the left ventricle and dysregulates vascular-derived neuro-regulatory genes. Aging leads to a down-regulation of miR-145 and de-repression of the neuro-repulsive factor Semaphorin-3A. miR-145 deletion, which increased Sema3a expression, or endothelial Sema3a overexpression reduced axon density, thus mimicking the observed aged heart phenotype. Removal of senescent cells, which accumulated with chronological age in parallel to the decline in nerve density, rescued age-induced denervation, reduced Sema3a expression, preserved heart rate variability and reduced electrical instability. These data suggest that senescence-associated regulation of neuro-regulatory genes is associated with reduced nerve density and, thereby, contributes to age-associated cardiac dysfunction.

2023-07-05 | E-MTAB-13093 | biostudies-arrayexpress

Spatially resolved multiomics of human cardiac niches - Multiome GEX

Project description:Using Multiome and previously published sc/snRNA-seq data, we studied eight anatomical regions of the human heart including left and right ventricular free walls (LV and RV), left and right atria (LA and RA), left ventricular apex (AX), interventricular septum (SP), sino-atrial node (SAN) and atrioventricular node (AVN). For the first time, we profile the cells of the human cardiac conduction system, revealing their distinctive repertoire of ion channels, G-protein coupled receptors and cell-cell interactions. We map the identified cells to spatial transcriptomic data to discover cellular niches within the eight regions of the heart.

2023-06-13 | E-MTAB-12916 | biostudies-arrayexpress

Spatially resolved multiomics of human cardiac niches - Multiome ATAC

2023-06-13 | E-MTAB-12919 | biostudies-arrayexpress

DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts

Project description:Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A) drive clonal hematopoiesis of indeterminate potential (CHIP) and are associated with adverse prognosis in patients with heart failure (HF). The interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential interaction partners of CHIP-mutated monocytes using combined transcriptomic data from peripheral blood mononuclear cells of HF patients with and without CHIP and cardiac tissue. We demonstrate that DNMT3A inactivation augments macrophage-to-cardiac fibroblasts interactions and induces cardiac fibrosis in mice and humans. Mechanistically, DNMT3A inactivation increases the release of heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) to activate cardiac fibroblasts. These findings not only identify a novel pathway of DNMT3A CHIP-driver mutation-induced instigation and progression of HF, but may also provide a rationale for the development of new anti-fibrotic strategies.

2023-10-20 | E-MTAB-13384 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Mouse Data)

Project description:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.

2021-05-13 | E-MTAB-10448 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Human Data)

2021-05-11 | E-MTAB-10432 | biostudies-arrayexpress

Joint single-cell/single-nucleus RNA-seq on hearts from healthy or HFpEF mice

Project description:In this project we explore the cellular heterogeneity of a mouse model of heart failure with preserved ejection fraction (HFpEF) involving a two-hit model of feeding a high fat diet (HFD) along with L-NAME administration. Healthy adult male mice (C57BL/6J inbred) were fed either a normal chow diet or HFD/L-NAME for 10 weeks or 15 weeks before performing sequencing experiments. Both cardiomyocytes (CMs) and total interstitial population (TIP) were captured using a protocol to jointly capture and sequence single-nuclei (for cardiomyocytes) and single-cells (for TIP) using the 10x Genomics Chromium system.

2024-05-08 | E-MTAB-13362 | biostudies-arrayexpress

Single-nucleus RNA-seq of liver tissue of 3 months old mice to investigate crosstalk between ploidy and zonation

Project description:Single-nucleus RNA-seq-2 method that allows deep characterization of nuclei isolated from frozen archived tissues. We have used this approach to characterize the transcriptional profile of individual hepatocytes with different levels of ploidy. This method has the potential to explore archived samples, for instance to study the development and progression of disease in complex tissues. To illustrate the potential of this method, we have deeply characterized the cellular heterogeneity driven by spatial distribution and different levels of ploidy in the young adult mouse liver.

2021-05-06 | E-MTAB-10223 | biostudies-arrayexpress

Single cell RNA-Seq of the mouse heart in response to chronic stress

Project description:We characterized single-cell transcriptional profiles of heart ventricles of C57BL/6J female and male mice subjected to a chronic stress, two weeks of continuous administration of Angiotensin II. The cell preparation we sequenced consisted of metabolically active, nucleated non-myocyte cells which were depleted of endothelial cells, mixed with nuclei isolated from cardiomyocytes. The goal of this experiment included characterizing cellular diversity in stressed and unstressed hearts, uncovering potential drivers of cardiac fibrosis and hypertrophy, and quantifying sexual dimorphism in cardiac gene expression.

2020-11-24 | E-MTAB-8810 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data