Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of engineered cardiac tissue in an oxygen gradient

ABSTRACT: Transcriptomic analysis of engineered cardiac tissue in an oxygen gradient

PROVIDER: PRJNA781583 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16975369.fastq.gz	Fastqsanger.gz
	SRR16975370.fastq.gz	Fastqsanger.gz
	SRR16975371.fastq.gz	Fastqsanger.gz
	SRR16975372.fastq.gz	Fastqsanger.gz
	SRR16975373.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Transcriptomic analysis of engineered cardiac tissue in an oxygen gradient

Project description:We report the use of RNA-seq for transcriptional analysis of engineered cardiac tissues cultured in microphysiological systems developed for tight control of oxygen levels, comparing normoxia, hypoxia, and a gradient divided into the normoxic side and hypoxic side.

2022-12-08 | GSE189108 | GEO

Transcriptional Remodeling in Human Cardiac Fibroblasts and Myocytes Induced by Oxygen-Dependent Crosstalk

Project description:Myocardial infarctions are caused by coronary occlusions that deprive downstream myocardial tissue of oxygenated blood, leading to localized necrosis of cardiac myocytes. Hypoxic injury drives a remodeling process in which cardiac fibroblasts activate and synthesize matrix proteins to form a scar. During this process, cardiac cells are exposed to an oxygen gradient at the infarct border zone that transitions from 0% oxygen at the site of injury to 10% oxygen in healthy myocardium. However, the impact of any crosstalk between hypoxic cardiac fibroblasts and neighboring, normoxic (10% oxygen) cardiac cells is unexplored because conventional research tools cannot re-create spatially heterogeneous oxygen landscapes. Here, we used a microfluidic device to co-culture hypoxic cardiac fibroblasts with (1) normoxic cardiac fibroblasts or (2) normoxic human induced pluripotent stem cell (hiPSC)-derived cardiac myocytes. We then compared their transcriptome to the same cells cultured in uniform hypoxia or normoxia. These data contribute to more advanced understanding of how oxygen-dependent crosstalk between cardiac cells impacts the wound healing process post-myocardial infarction.

2024-06-30 | GSE254962 | GEO

Lactate and Immunomagnetic-purified iPSC-derived Cardiomyocytes Generate Comparable Engineered Cardiac Tissue Constructs

Project description:top down and bottom up proteomics files for Lactate and Immunomagnetic-purified iPSC-derived Cardiomyocytes Generate Comparable Engineered Cardiac Tissue Constructs

2023-05-05 | MSV000091869 | MassIVE

Phenotypic variation between stromal cells differentially impacts engineered cardiac tissue function

Project description:Understanding the relationship between parenchymal and supporting cell populations is paramount to recapitulate the multicellular complexity of native tissues. Incorporation of stromal cells is widely recognized to be necessary for the stable formation of stem cell-derived cardiac tissues, yet the types of stromal cells used has varied widely. This study systematically characterized several stromal populations and found that stromal phenotype and morphology was highly variable depending on cell source and exerted differential impacts on cardiac tissue function and iPSC-CM phenotype. Therefore, the choice of supporting stromal population can differentially impact the phenotypic or functional performance of engineered cardiac tissues.

2019-03-30 | GSE129058 | GEO

Macrophages enhance contractile force in iPSC-derived human engineered cardiac tissue

Project description:Resident cardiac macrophages are critical mediators of cardiac function. Despite their known importance to cardiac electrophysiology and tissue maintenance, there are currently no stem-cell derived models of human engineered cardiac tissues (hECT) that include resident macrophages. In this study, we made an iPSC-derived hECT model with a resident population of macrophages (iM0) to better recapitulate the native myocardium, and characterized their impact on tissue function. Macrophage retention within the hECTs was confirmed via immunofluorescence after 28 days of cultivation. Inclusion of iM0 significantly impacted hECT function, increasing contractile force production. A potential mechanism underlying these changes was revealed by interrogation of calcium signaling, which demonstrated modulation of β-adrenergic signaling in +iM0 hECTs. Collectively, these findings demonstrate that macrophages significantly enhance cardiac function in iPSC-derived hECT models, emphasizing the need to further explore their contributions not only in healthy hECT models, but also in the contexts of disease and injury.

2024-05-10 | GSE266797 | GEO

A laboratory-based model ecosystem reveals genetic determinants of methanotroph phenotypic heterogeneity in a methane-oxygen counter gradient

Project description:Connecting genes to phenotypic traits in bacteria is often challenging because of a lack of environmental cues in laboratory settings. However, laboratory-based model ecosystems offer a means to better account for natural conditions compared to standard planktonic cultures, aiding in the linking of genotypes and phenotypes. Here, we present a simple, cost-effective, laboratory-based model ecosystem to study aerobic methane-oxidizing bacteria (methanotrophs). This system, referred to as the gradient syringe, is made by inoculating bacteria into semi-solid agarose held within a disposable syringe. Empty space at one end of the syringe is flushed with methane gas, while the other end is open to the atmosphere through a sterile filter. We show this system replicates the methane-oxygen counter gradient typically found in the natural soil environment of methanotrophs. Culturing the methanotroph Methylomonas sp. strain LW13 in this system produced a distinct horizontal band at the intersection of the counter gradient, which we discovered was due not to increased cell growth at this location but instead to an increased amount of extracellular polymeric substances (EPS). We also discovered that different methanotrophic taxa formed EPS bands with distinct locations and morphologies when grown in the methane-oxygen counter gradient. By comparing transcriptomic data from LW13 growing within and surrounding this EPS band, we identified genes implicated in cell growth and EPS formation within the gradient syringe, and validated the involvement of these genes with knockout strains. This work highlights the use of a laboratory-based model ecosystem that more closely mimics the natural environment to uncover methanotroph phenotypes missing from standard planktonic cultures, and link these phenotypes their genetic determinants.

2023-10-05 | GSE243827 | GEO

Phenotypic variation between stromal cells differentially impacts engineered cardiac tissue function

Project description:Phenotypic variation between stromal cells differentially impacts engineered cardiac tissue function

| PRJNA529887 | ENA

Macrophages enhance contractile force in iPSC-derived human engineered cardiac tissue

Project description:Macrophages enhance contractile force in iPSC-derived human engineered cardiac tissue

| PRJNA1108328 | ENA

Transcriptomic profileing of iPSC-derived engineered cardiac tissue in which cMyBP-C have been ablated in the heterozygous and homozygous states on an isogenic background

Project description:Truncation mutations in cardiac myosin binding protein C (cMyBP-C), are common causes of hypertrophic cardiomyopathy (HCM). Heterozygous carriers present with classical HCM, while homozygous carriers present with early onset HCM that rapidly progress to heart failure. We used CRISPR-Cas9 to introduce heterozygous (cMyBP-C+/-) and homozygous (cMyBP-C-/-) frame-shift mutations into MYBPC3 in human iPSCs. Cardiomyocytes derived from these isogenic lines were used to generate engineered cardiac tissue constructs (ECTs). RNAseq analysis on 14 day old ECTs revealed enrichment of differentially expressed hypertrophic, sarcomeric, Ca2+-handling and metabolic genes in cMyBP-C+/- and cMyBP-C-/- ECTs.

2023-02-23 | GSE224129 | GEO

Transcriptome analysis of cardiac tissues from mice subjected to SD model with oxygen therapy

Project description:Adequate sleep is essential for relieving stress and rejuvenating the mind; however, undesirable physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly common. However, the influence of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially on cardiac diseases remain controversial. Here, we constructed the experimental SD model in mice and found it significantly resulted in weakness, depression-like behaviors, and multiple organs dysfunction. Intriguingly, SD mice developed pathogenic cardiac hypertrophy and fibrosis with poor ejection fraction as well as fractional shortening. 16s rRNA sequencing demonstrated that SD-induced the pathogenic effects of gut microbiota, which was also observed in mice received by fecal microbe from SD mice in fecal microbiota transplantation (FMT) assays. Next, we investigated the therapeutic effects and underlying mechanisms of oxygen therapy in gut microbiota-associated cardiac fibrosis and dysfunction. The environment of 30% oxygen concentration effectively ameliorated the pathological effects on cardiac function. Transcriptome data also found oxygen therapy targeted several hypoxia-dependent pathways and suppressed cardiac collagen production. In conclusion, these results indicated the importance of sufficient sleep in gut microbiota and may represent a potential therapeutic strategy of oxygen environment exerts protective effects in sleepless sufferings through gut microbiota.

2025-03-25 | GSE284746 | GEO

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