Human pluripotent stem cell-derived cardiomyocyte maturation both in vivo and in vitro
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ABSTRACT:
PROVIDER: PRJNA788438 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
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| SRR17216919.fastq.gz | Fastqsanger.gz | |||
| SRR17216920.fastq.gz | Fastqsanger.gz | |||
| SRR17216921.fastq.gz | Fastqsanger.gz | |||
| SRR17216922.fastq.gz | Fastqsanger.gz | |||
| SRR17216923.fastq.gz | Fastqsanger.gz |
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Project description:The mammalian heart undergoes maturation during postnatal life to meet the increased functional requirements of the adult. However, the key drivers of this process remain poorly defined. We developed as 96-well screening platform, using human pluripotent stem cell derived cardiac organoids, to determine the molecular requirements for in vitro cardiomyocyte maturation. Here, we describe gene expression changes resulting from culturing human cardiac organoids in standard cell culture conditions and under optimized maturation conditions. We assessed our maturation conditions by comparing transcriptional changes of human cardiac organoids to RNA isolated from human heart. Interesting, analysis of these data revealed that a switch to fatty acid oxidative metabolism is a key governor of cardiomyocyte maturation and mature cardiac organoids were refractory to mitogenic stimuli.
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Project description:Cardiomyocyte maturation is the final stage of heart development, and abnormal cardiomyocyte maturation will lead to serious heart diseases. CXXC zinc finger protein 1 (Cfp1) is an important epigenetic factor, which plays an essential role in the development and maturation of multi-lineage cells, while its effect on the maturation of cardiomyocyte remains unclear. This study was performed to explore the potential role of Cfp1 in cardiomyocyte maturation of heart and the underlying mechanisms. Cardiomyocyte-specific Cfp1 knockout (Cfp1-cKO) mice died within 4 weeks of birth. Cardiomyocytes from Cfp1-cKO mice showed an inhibited maturation phenotype in structure, metabolism, contractile function, and cell cycle, accompanied by down-regulation of adult genes and up-regulation of fetal genes. In contrast, cardiomyocyte-specific Cfp1 transgenic (Cfp1-TG) mice and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) overexpressing Cfp1 showed a more mature phenotype. Mechanistically, deficiency of Cfp1 results in reduced trimethylation on lysine 4 of histone H3 (H3K4me3) modification and formation of ectopic H3K4me3. Moreover, Cfp1 deletion decreased the level of H3K4me3 modification in adult genes and increased the level of H3K4me3 modification in fetal genes. Collectively, Cfp1 modulates the expression of cardiomyocyte maturation related genes by modulating histone H3K4me3 modification, which in turn regulates cardiomyocyte maturation. This study implicates Cfp1 as an important molecule regulating cardiomyocyte maturation, and its dysfunction is strongly associated with cardiac disease.
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Project description:AP-1 activation mediates postnatal cardiomyocyte maturation
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Project description:Cardiomyocytes and cardiac fibroblasts undergo coordinated maturation after birth, and cardiac fibroblasts are required for postnatal cardiomyocyte maturation in mice. Here, we investigate the role of cardiac fibroblast-expressed Growth Differentiating Factor 10 (GDF10) in postnatal heart development. In neonatal mice, Gdf10 is expressed specifically in cardiac fibroblasts, with its highest expression coincident with onset of cardiomyocytes cell cycle arrest and transition to hypertrophic growth. In neonatal rat ventricular myocyte cultures, GDF10 treatment promotes cardiomyocyte maturation indicated by increased binucleation, downregulation of cell cycle progression genes and upregulation of cell cycle inhibitor genes. GDF10 treatment leads to an increase in cardiomyocyte cell size together with increased expression of mature sarcomeric protein isoforms and decreased expression of fetal cardiac genes. RNAsequencing of GDF10-treated NRVM shows an increase in gene expression related to myocardial maturation, including upregulation of sodium and potassium channel genes. In vivo, loss of Gdf10 leads to a delay in myocardial maturation indicated by a decrease in cardiomyocyte cell size and binucleation as well as increased mitotic activity at postnatal (P) day 7. Further, induction of mature sarcomeric protein isoform gene expression is delayed, and expression of cell cycle progression genes is prolonged. However, by P10 indicators of cardiomyocyte maturation and mitotic activity are normalized in Gdf10-null hearts relative to controls. Together, these results implicate Gdf10 as a novel crosstalk mediator between cardiomyocytes and cardiac fibroblasts, required for appropriate timing of cardiomyocyte maturation steps including binucleation, hypertrophy, mature sarcomeric isoform switch and cell cycle arrest in the postnatal period.
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