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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

ABSTRACT: Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

PROVIDER: PRJNA421012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6345651.fastq.gz	Fastqsanger.gz
	SRR6345652.fastq.gz	Fastqsanger.gz
	SRR6345653.fastq.gz	Fastqsanger.gz
	SRR6345654.fastq.gz	Fastqsanger.gz

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

Project description:Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

Project description:To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration.

2018-01-02 | GSE107678 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration.

Project description:The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 (miR-128) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of miR-128 impairs CM proliferation and cardiac function, while miR-128 deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses p27 (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2. Furthermore, deletion of miR-128 promotes cell cycle re-entry of adult CMs, thereby reducing the levels of fibrosis, and attenuating cardiac dysfunction in response to MI. These results suggest that miR-128 serves as a critical regulator of endogenous CM proliferation, and might be a novel therapeutic target for heart repair.

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α-Ketoglutarate Promotes Cardiomyocyte Proliferation and Heart Regeneration after Myocardial Infarction

Project description:The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal (P) day 7. How to stimulate the adult cardiomyocyte to re-enter the cell cycle is still unknown. Accumulating evidence suggests that cardiomyocyte proliferation depends on its metabolic state. Due to the tight connection between the tricarboxylic acid cycle (TCA) and cell proliferation, we analyzed the TCA metabolites between P0.5 and P7 mouse hearts and found that α-ketoglutarate (α-KG) ranked first among the decreased metabolites. The intraperitoneal injection of exogenous α-KG extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction (MI) by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-KG levels. Mechanistically, α-KG activates Jmjd3, a histone lysine demethylase, that decreases H3K27me3 expression and deposition of H3K4me3 at the promoters of cell cycle and structural maturation genes in cardiomyocytes. Our present study shows that α-KG promotes cardiomyocyte proliferation by Jmjd3-dependent demethylation and inactivation of H3K27me3 andH3K4me3, which is a potential therapeutic approach for treating MI and heart failure.

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Project description:Fibroblasts are activated to repair the heart following injury. Fibroblast activation in the mammalian heart leads to a permanent fibrotic scar that impairs cardiac function. In other organisms, such as zebrafish, cardiac injury is followed by transient fibrosis and scar-free regeneration. The mechanisms that drive scarring versus scar-free regeneration are not well understood. Here, we show that the homeobox-containing transcription factor Prrx1b is required for scar-free regeneration of the zebrafish heart as the loss of Prrx1b results in excessive fibrosis and impaired cardiomyocyte proliferation. Through lineage tracing and single-cell RNA sequencing we find that Prrx1b is activated in epicardial-derived cells where it restricts TGFβ ligand expression and collagen production. Furthermore, through combined in vitro experiments in human fetal epicardial-derived cells and in vivo rescue experiments in zebrafish, we conclude that Prrx1 stimulates Nrg1 expression and promotes cardiomyocyte proliferation. Collectively, these results indicate that Prrx1 is a key transcription factor that balances fibrosis and regeneration in the injured zebrafish heart.

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