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AP-1 activation mediates postnatal cardiomyocyte maturation

ABSTRACT: AP-1 activation mediates postnatal cardiomyocyte maturation

PROVIDER: PRJNA756241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15526400_1.fastq.gz	Fastqsanger.gz
	SRR15526400_2.fastq.gz	Fastqsanger.gz
	SRR15526401_1.fastq.gz	Fastqsanger.gz
	SRR15526401_2.fastq.gz	Fastqsanger.gz
	SRR15526402_1.fastq.gz	Fastqsanger.gz

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AP-1 activation mediates postnatal cardiomyocyte maturation

Project description:Mammalian cardiomyocytes rapidly mature after birth, with hallmarks such as cell-cycle exit, binucleation, and metabolic switch to oxidative phosphorylation of lipids. The causes and transcriptional programs regulating cardiomyocyte maturation are not fully understood yet. Thus, we performed single cell RNA-seq of neonatal and postnatal day 7 rat hearts to identify the key factors for this process and found AP-1 as a key factor to regulate cardiomyocyte maturation. To find the mechanism of AP-1 during cardiomyocyte maturation, we performed RNA-seq analysis of neonatal rat ventricular cardiomyocytes and found Ap-1 promote cardiomyocyte maturation by regulating cardiomyocyte metabolism.

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Postnatal development of Cardiomyocyte

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Single-Cell RNA-seq of Postnatal Development of Cardiomyocyte

Project description:Postnatal heart maturation is the basis of normal cardiac function and provides critical insights into heart repair and regenerative medicine. While static snapshots of the maturing heart have provided much insight into its molecular signatures, few key events during postnatal cardiomyocyte maturation have been uncovered.Here we processed single cell RNASeq of Cardiomyocyte at different postnatal time points.

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Postnatal development of Cardiomyocyte

Project description:Postnatal development of Cardiomyocyte

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Single cell analysis of murine fibroblasts identifies neonatal to adult switching that regulates cardiomyocyte maturation

Project description:Cardiac maturation lays the foundation for postnatal heart development and disease, yet little is known about the contributions of the microenvironment to cardiomyocyte maturation. By integrating single-cell RNA-sequencing data of mouse hearts at multiple postnatal stages, we construct cellular interactomes and regulatory signaling networks. Here we report switching of fibroblast subtypes from a neonatal to adult state and this drives cardiomyocyte maturation. Molecular and functional maturation of neonatal mouse cardiomyocytes and human embryonic stem cell-derived cardiomyocytes are considerably enhanced upon coculture with corresponding adult cardiac fibroblasts. Further, single-cell analysis of in vivo and in vitro cardiomyocyte maturation trajectories identify highly conserved signaling pathways, pharmacological targeting of which substantially delays cardiomyocyte maturation in postnatal hearts, and markedly enhances cardiomyocyte proliferation and improves cardiac function in infarcted hearts. Together, we identify cardiac fibroblasts as a key constituent in the microenvironment promoting cardiomyocyte maturation, providing insights into how the manipulation of cardiomyocyte maturity may impact on disease development and regeneration.

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The tRNA methyltransferase Mettl1 governs ketogenesis through translational regulation and drives metabolic reprogramming in cardiomyocyte maturation

Project description:Following birth, the heart undergoes intricate transitions in response to the altered environment, including shifts in energy metabolism and cytoarchitecture, such as the switch from glucose to lipid utilization and the transformation of fetal-to-adult sarcomeric gene isoforms, all aimed at achieving functional maturation. These adaptations facilitate efficient energy production and cardiac contraction, enabling the heart to effectively pump blood throughout the body. Although the early postnatal period is widely recognized as a critical phase for cardiomyocyte maturation, the precise mechanisms initiating and orchestrating this process remain elusive. Using in vivo and in vitro models incorporated with multi-omic analyses, we here show that Mettl1 is a critical regulator in postnatal cardiomyocyte maturation. We demonstrate that Mettl1 is required for the proper ketogenesis in cardiomyocyte maturation via regulating Hmgcs2 translation. Loss of Mettl1 leads to aberrant metabolic reprogramming and subsequent cardiomyocyte immaturation through the deficiency in lysine β-hydroxybutyrylation of TCA cycle-related proteins.

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Postnatal lipids drive hepatocyte maturation

Project description:Postnatal lipids drive hepatocyte maturation

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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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AP-1 Regulates Chromatin Accessibility to Promote Sarcomere Disassembly and Cardiomyocyte Protrusion during Zebrafish Heart Regeneration

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Project description:Retinoic acid (RA), the major active metabolite of vitamin A, is essential for organogenesis, homeostasis, and tissue morphogenesis. Despite the importance of RA signaling in embryo heart development, little is known about its function in the early postnatal period. For a comprehensive transcriptional evaluation of the effect of RA signaling on neonatal cardiomyocyte cell cycle arrest and maturation, we performed RNA-seq analysis of cultured perinatal cardiomyocytes treated with all-trans retinoic acid (ATRA) in vitro.

2024-08-13 | GSE263096 | GEO

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