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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

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			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

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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.

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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.

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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.

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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.

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

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